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    MGMT testing--the challenges for biomarker-based glioma treatment. Wick Wolfgang,Weller Michael,van den Bent Martin,Sanson Marc,Weiler Markus,von Deimling Andreas,Plass Christoph,Hegi Monika,Platten Michael,Reifenberger Guido Nature reviews. Neurology Many patients with malignant gliomas do not respond to alkylating agent chemotherapy. Alkylator resistance of glioma cells is mainly mediated by the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT). Epigenetic silencing of the MGMT gene by promoter methylation in glioma cells compromises this DNA repair mechanism and increases chemosensitivity. MGMT promoter methylation is, therefore, a strong prognostic biomarker in paediatric and adult patients with glioblastoma treated with temozolomide. Notably, elderly patients (>65-70 years) with glioblastoma whose tumours lack MGMT promoter methylation derive minimal benefit from such chemotherapy. Thus, MGMT promoter methylation status has become a frequently requested laboratory test in neuro-oncology. This Review presents current data on the prognostic and predictive relevance of MGMT testing, discusses clinical trials that have used MGMT status to select participants, evaluates known issues concerning the molecular testing procedure, and addresses the necessity for molecular-context-dependent interpretation of MGMT test results. Whether MGMT promoter methylation testing should be offered to all individuals with glioblastoma, or only to elderly patients and those in clinical trials, is also discussed. Justifications for withholding alkylating agent chemotherapy in patients with MGMT-unmethylated glioblastomas outside clinical trials, and the potential role for MGMT testing in other gliomas, are also discussed. 10.1038/nrneurol.2014.100
    Ionizing radiation and the risk of brain and central nervous system tumors: a systematic review. Braganza Melissa Z,Kitahara Cari M,Berrington de González Amy,Inskip Peter D,Johnson Kimberly J,Rajaraman Preetha Neuro-oncology Although exposure to moderate-to-high doses of ionizing radiation is the only established environmental risk factor for brain and CNS tumors, it is not clear whether this relationship differs across tumor subtypes, by sex or age at exposure, or at the low-to-moderate range of exposure. This systematic review summarizes the epidemiologic evidence on the association between ionizing radiation exposure and risk of brain/CNS tumors. Articles included in this review estimated radiation exposure doses to the brain and reported excess relative risk (ERR) estimates for brain/CNS tumors. Eight cohorts were eligible for inclusion in the analysis. Average age at exposure ranged from 8 months to 26 years. Mean dose to the brain ranged from 0.07 to 10 Gy. Elevated risks for brain/CNS tumors were consistently observed in relation to ionizing radiation exposure, but the strength of this association varied across cohorts. Generally, ionizing radiation was more strongly associated with risk for meningioma compared with glioma. The positive association between ionizing radiation exposure and risk for glioma was stronger for younger vs older ages at exposure. We did not observe an effect modification on the risk for meningioma by sex, age at exposure, time since exposure, or attained age. The etiologic role of ionizing radiation in the development of brain/CNS tumors needs to be clarified further through additional studies that quantify the association between ionizing radiation and risk for brain/CNS tumors at low-to-moderate doses, examine risks across tumor subtypes, and account for potential effect modifiers. 10.1093/neuonc/nos208
    Exposure to lead increases the risk of meningioma and brain cancer: A meta-analysis. Meng Yu,Tang Caoli,Yu Jun,Meng Shiyao,Zhang Wanying Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) OBJECTIVE:To analyze the relationship between environmental lead exposure and various types of brain tumors. METHODS:Search databases PubMed, Web of Science, Embase and Chinese National Knowledge Infrastructure (CNKI) as of July 1, 2019. Stata 15.0 software was used for analysis. RESULTS:In the case control, lead exposure was associated with gliomas and meningiomas 0.82 (95 % CI: 0.69, 0.95) and 1.06 (95 % CI: 0.65, 1.46). In the cohort study, lead exposure was associated with brain cancer and meningiomas 1.07 (95 % CI: 0.95, 1.19) and 1.06 (95 % CI: 0.94, 1.17). The risk of childhood brain tumors associated with parental lead exposure was 1.17 (95 % CI: 0.99, 1.34). CONCLUSIONS:Lead may be a risk factor for meningiomas and brain cancers. However, the glioma results suggest that lead may be a protective factor, which needs to be further studied. 10.1016/j.jtemb.2020.126474
    [Gliomas: the role of environmental risk factors and genetic predisposition]. Houben M P W A,van Duijn C M,Coebergh J W W,Tijssen C C Nederlands tijdschrift voor geneeskunde Exposure to ionising radiation is the only established risk factor for glioma. Although gliomas are looked upon as a non-heritable disease, physicians regularly see patients with affected relatives in practice. A few monogenetic tumour syndromes explain < 5% of all gliomas: neurofibromatosis type 1 and 2, Li-Fraumeni syndrome, tuberous sclerosis, Turcot syndrome, Gorlin syndrome, and the melanomaastrocytoma syndrome. Aggregation ofgliomas in families without these tumour syndromes also occurs. The overall familial pattern is generally atypical for hereditary cancers. Relatives are estimated to have a 2- to 9-fold increased risk. The occurrence ofgliomas in families can probably best be explained by a multifactorial model: environmental risk factors with a genetically determined susceptibility for these risk factors. The identity of the genetic variants leading to this predisposition remains to be determined. When there are indications of a hereditary tumour syndrome, additional diagnostic investigation is indicated.
    Modulation of glioma risk and progression by dietary nutrients and antiinflammatory agents. Kyritsis Athanassios P,Bondy Melissa L,Levin Victor A Nutrition and cancer Gliomas are tumors of glial origin formed in the central nervous system and exhibit profound morphological and genetic heterogeneity. The etiology of this heterogeneity involves an interaction between genetic alterations and environmental risk factors. Scientific evidence suggests that certain natural dietary components, such as phytoestrogens, flavonoids, polyunsaturated fatty acids, and vitamins, may exert a protective effect against gliomas by changing the nature of the interaction between genetics and environment. Similarly, certain antiinflammatory drugs and dietary modifications, such as methionine restriction and the adoption of low-calorie or ketogenic diets, may take advantage of glioma and normal glial cells' differential requirements for glucose, methionine, and ketone bodies and may, therefore, be effective as part of preventive or treatment strategies for gliomas. Treatment trials of glioma patients and chemoprevention trials of individuals with a known genetic predisposition to glioma using the most promising of these agents, such as the antiinflammatory drugs curcumin and gamma-linolenic acid, are needed to validate or refute these agents' putative role in gliomas. 10.1080/01635581.2011.523807
    Red and processed meat consumption and risk of glioma in adults: A systematic review and meta-analysis of observational studies. Saneei Parvane,Willett Walter,Esmaillzadeh Ahmad Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences BACKGROUND:These findings from several observational studies, investigated the association between red meat consumption and gliomas, were inconsistent. We conducted a systematic review and meta-analysis of observational studies to summarize available date on the relation between meat intake and risk of glioma. MATERIALS AND METHODS:A systematic literature search of relevant reports published until May 2014 of the PubMed/Medline, ISI Web of Knowledge, Excerpta Medica database, Ovid database, Google Scholar, and Scopus databases was conducted. From 723 articles yielded in the preliminary literature search, data from eighteen publications (14 case-control, three cohort, and one nested case-control study) on unprocessed red meat, processed meat, and/or total red meat consumption in relation to glioma in adults were included in the analysis. Quality assessment of studies was performed. Random effects model was used to conduct the meta-analysis. RESULTS:We found a positive significant association between unprocessed red meat intake and risk of glioma (relative risk [RR] = 1.30; 95% confidence interval [CI]: 1.08-1.58) after excluding three studies with uncertain type of brain cancer. This analysis included only one cohort study which revealed no relation between unprocessed red meat intake and glioma (RR = 1.75; 95% CI: 0.35-8.77). Consumption of processed meats was not related to increased risk of glioma in population-based case-control studies (RR = 1.26; 95% CI: 1.05-1.51) and reduced risk in hospital-based case-controls (RR = 0.79; 95% CI: 0.65-0.97). No significant association was seen between processed red meat intake and risk of glioma in cohort studies (RR: 1.08; 95% CI: 0.84-1.37). Total red meat consumption was not associated with risk of adult glioma in case-control or cohort studies. CONCLUSION:In this meta-analysis of 18 observational studies, we found a modest positive association between unprocessed red meat intake and risk of gliomas based almost entirely on case-control studies. Processed red meat was overall not associated with risk of gliomas in case-control or cohort studies. 10.4103/1735-1995.165970
    Association between common polymorphisms in ERCC gene and glioma risk: A meta-analysis of 15 studies. Qian Tengda,Zhang Bin,Qian Chunsheng,He Yunwen,Li Yihuan Medicine BACKGROUND:A number of studies have investigated the roles of excision repair cross complementation group 1 (ERCC1), ERCC2, and ERCC5 genes polymorphisms in the development of glioma; however, the results were inconsistent. Here, we performed a meta-analysis to investigate the association between 6 polymorphisms in the ERCC genes (rs3212986, rs11615, rs13181, rs1799793, rs238406, rs17655) and glioma risk. METHODS:The PubMed, Embase, and Web of science were searched up to September 6, 2016, for studies on the association between ERCC polymorphisms and glioma risk. A fixed-effects or random-effects model was used to calculate the pooled odds ratios based on the results from the heterogeneity tests. Sensitivity and cumulative meta-analyses were also performed. RESULTS:A total of 15 studies were eligible for the pooled analysis, conducted in 2 populations of ethnic descent: 8 Europeans and 7 Asians. The results showed that ERCC1 rs3212986 polymorphism was positively associated with glioma [AA vs CC: odds ratio (OR) = 1.298, 95% confidence interval (95% CI) = 1.043-1.230, P = .025]. Association of the ERCC2 rs13181 and rs1799793 polymorphisms was only observed in Asians (CC vs AA for rs13181: OR = 1.539, 95% CI = 1.122-2.109, P = .007; AA vs GG for rs1799793: OR = 1.474, 95% CI = 1.090-1.994, P = .012). However, no association was observed between glioma risk and ERCC1 rs11615, ERCC2 rs238406, and ERCC5 rs17655 polymorphisms. Moreover, sensitivity and cumulative meta-analyses confirmed the stability of the results. CONCLUSIONS:Our meta-analysis indicated that the ERCC1 rs3212986 polymorphism and 2 polymorphisms in ERCC2 gene (rs13181 and rs1799793) contributed to the susceptibility of glioma. 10.1097/MD.0000000000006832
    Genetic and molecular epidemiology of adult diffuse glioma. Molinaro Annette M,Taylor Jennie W,Wiencke John K,Wrensch Margaret R Nature reviews. Neurology The WHO 2007 glioma classification system (based primarily on tumour histology) resulted in considerable interobserver variability and substantial variation in patient survival within grades. Furthermore, few risk factors for glioma were known. Discoveries over the past decade have deepened our understanding of the molecular alterations underlying glioma and have led to the identification of numerous genetic risk factors. The advances in molecular characterization of glioma have reframed our understanding of its biology and led to the development of a new classification system for glioma. The WHO 2016 classification system comprises five glioma subtypes, categorized by both tumour morphology and molecular genetic information, which led to reduced misclassification and improved consistency of outcomes within glioma subtypes. To date, 25 risk loci for glioma have been identified and several rare inherited mutations that might cause glioma in some families have been discovered. This Review focuses on the two dominant trends in glioma science: the characterization of diagnostic and prognostic tumour markers and the identification of genetic and other risk factors. An overview of the many challenges still facing glioma researchers is also included. 10.1038/s41582-019-0220-2
    The Influence of Nutritional and Lifestyle Factors on Glioma Incidence. Bielecka Joanna,Markiewicz-Żukowska Renata Nutrients Cancers are the first main cause of premature death in developed countries. Since brain tumors, especially gliomas, are the most lethal type of cancers, risk factors for their prevalence are still being discussed. Nearly 30-50% of all cancers could be prevented by proper nutritional habits and other lifestyle factors, but their influence on the tumors of the central nervous system has not been explained completely and still requires further studies. That is why we attempted to review the available research in this field, with a special focus on the factors with the proven protective activity observed in other cancers. Adequate vegetables and antioxidants (such as vitamins C and A) provided with a diet could have a protective effect, while other factors have shown no correlation with the incidence of glioma. However, further studies are necessary to determine whether fish, coffee, and tea consumption may prevent glioma. Maintaining proper body weight and undertaking a sufficient level of daily physical activity also seem to be important. Excessive body mass index (BMI) and higher attained height have increased the risk of glioma. In order to link more accurately the chosen factors to the prevalence of gliomas, it seems necessary to conduct large cohort, prospective, controlled studies in different world regions. 10.3390/nu12061812
    Risk factors for childhood and adult primary brain tumors. Ostrom Quinn T,Adel Fahmideh Maral,Cote David J,Muskens Ivo S,Schraw Jeremy M,Scheurer Michael E,Bondy Melissa L Neuro-oncology Primary brain tumors account for ~1% of new cancer cases and ~2% of cancer deaths in the United States; however, they are the most commonly occurring solid tumors in children. These tumors are very heterogeneous and can be broadly classified into malignant and benign (or non-malignant), and specific histologies vary in frequency by age, sex, and race/ethnicity. Epidemiological studies have explored numerous potential risk factors, and thus far the only validated associations for brain tumors are ionizing radiation (which increases risk in both adults and children) and history of allergies (which decreases risk in adults). Studies of genetic risk factors have identified 32 germline variants associated with increased risk for these tumors in adults (25 in glioma, 2 in meningioma, 3 in pituitary adenoma, and 2 in primary CNS lymphoma), and further studies are currently under way for other histologic subtypes, as well as for various childhood brain tumors. While identifying risk factors for these tumors is difficult due to their rarity, many existing datasets can be leveraged for future discoveries in multi-institutional collaborations. Many institutions are continuing to develop large clinical databases including pre-diagnostic risk factor data, and developments in molecular characterization of tumor subtypes continue to allow for investigation of more refined phenotypes. Key Point 1. Brain tumors are a heterogeneous group of tumors that vary significantly in incidence by age, sex, and race/ethnicity.2. The only well-validated risk factors for brain tumors are ionizing radiation (which increases risk in adults and children) and history of allergies (which decreases risk).3. Genome-wide association studies have identified 32 histology-specific inherited genetic variants associated with increased risk of these tumors. 10.1093/neuonc/noz123
    Environmental risk factors of primary brain tumors: A review. Vienne-Jumeau A,Tafani C,Ricard D Revue neurologique Adult primary tumors of the central nervous system are rare, but the incidence is increased in some European countries. Several environmental exposures have been investigated as potential risk factors, but for most, scientific evidence is still lacking. Here we review studies of environmental factors potentially involved in the carcinogenesis of brain tumors: the potential association between primary central nervous system tumors and ionizing radiation, some toxic agents (N-nitroso compounds, pesticides), air pollution, and radiofrequency electromagnetic waves. Brain-ionizing irradiation, especially during childhood, constitutes a well-established risk factor for brain tumors. Exposure to environmental toxins has been poorly explored and data give inconsistent clues about N-nitroso compounds or pesticides as risk factors of brain tumors even for prenatal exposure. For out-door pollution and risk of brain tumour, results of large prospective studies are contradictory. The effect of mobile phones on the risk of developing brain tumors has not been established for glioma and meningioma in adults, but the link with acoustic neurinoma is becoming robust. The effect of mobile phones has still not been explored in children. 10.1016/j.neurol.2019.08.004
    Height in adolescence as a risk factor for glioma subtypes: a nationwide retrospective cohort study of 2.2 million subjects. Tschernichovsky Roi,Katz Lior H,Derazne Estela,Berliner Matan Ben-Zion,Simchoni Maya,Levine Hagai,Keinan-Boker Lital,Benouaich-Amiel Alexandra,Kanner Andrew A,Laviv Yosef,Honig Asaf,Dudnik Elizabeth,Siegal Tali,Mandel Jacob,Twig Gilad,Yust-Katz Shlomit Neuro-oncology BACKGROUND:Gliomas manifest in a variety of histological phenotypes with varying aggressiveness. The etiology of glioma remains largely unknown. Taller stature in adulthood has been linked with glioma risk. The aim of this study was to discern whether this association can be detected in adolescence. METHODS:The cohort included 2 223 168 adolescents between the ages of 16 and 19 years. Anthropometric measurements were collected at baseline. Incident cases of glioma were extracted from the Israel National Cancer Registry over a follow-up period spanning 47 635 745 person-years. Cox proportional hazard models were used to estimate the hazard ratio (HR) for glioma and glioma subtypes according to height, body mass index (BMI), and sex. RESULTS:A total of 1195 patients were diagnosed with glioma during the study period. Mean (SD) age at diagnosis was 38.1 (11.7) years. Taller adolescent height (per 10-cm increase) was positively associated with the risk for glioma of any type (HR: 1.15; P = .002). The association was retained in subgroup analyses for low-grade glioma (HR: 1.17; P = .031), high-grade glioma (HR: 1.15; P = .025), oligodendroglioma (HR: 1.31; P = .015), astrocytoma (HR: 1.12; P = .049), and a category of presumed IDH-mutated glioma (HR: 1.17; P = .013). There was a trend toward a positive association between height and glioblastoma, however this had borderline statistical significance (HR: 1.15; P = .07). After stratification of the cohort by sex, height remained a risk factor for men but not for women. CONCLUSIONS:The previously established association between taller stature in adulthood and glioma risk can be traced back to adolescence. The magnitude of association differs by glioma subtype. 10.1093/neuonc/noab049
    Risks of carcinogenesis from electromagnetic radiation of mobile telephony devices. Yakymenko I,Sidorik E Experimental oncology Intensive implementation of mobile telephony technology in everyday human life during last two decades has given a possibility for epidemiological estimation of long-term effects of chronic exposure of human organism to low-intensive microwave (MW) radiation. Latest epidemiological data reveal a significant increase in risk of development of some types of tumors in chronic (over 10 years) users of mobile phone. It was detected a significant increase in incidence of brain tumors (glioma, acoustic neuroma, meningioma), parotid gland tumor, seminoma in long-term users of mobile phone, especially in cases of ipsilateral use (case-control odds ratios from 1.3 up to 6.1). Two epidemiological studies have indicated a significant increase of cancer incidence in people living close to the mobile telephony base station as compared with the population from distant area. These data raise a question of adequacy of modern safety limits of electromagnetic radiation (EMR) exposure for humans. For today the limits were based solely on the conception of thermal mechanism of biological effects of RF/MW radiation. Meantime the latest experimental data indicate the significant metabolic changes in living cell under the low-intensive (non-thermal) EMR exposure. Among reproducible biological effects of low-intensive MWs are reactive oxygen species overproduction, heat shock proteins expression, DNA damages, apoptosis. The lack of generally accepted mechanism of biological effects of low-intensive non-ionizing radiation doesn't permit to disregard the obvious epidemiological and experimental data of its biological activity. Practical steps must be done for reasonable limitation of excessive EMR exposure, along with the implementation of new safety limits of mobile telephony devices radiation, and new technological decisions, which would take out the source of radiation from human brain.
    Overexpression of isocitrate dehydrogenase mutant proteins renders glioma cells more sensitive to radiation. Li Sichen,Chou Arthur P,Chen Weidong,Chen Ruihuan,Deng Yuzhong,Phillips Heidi S,Selfridge Julia,Zurayk Mira,Lou Jerry J,Everson Richard G,Wu Kuan-Chung,Faull Kym F,Cloughesy Timothy,Liau Linda M,Lai Albert Neuro-oncology Mutations in isocitrate dehydrogenase 1 (IDH1) or 2 (IDH2) are found in a subset of gliomas. Among the many phenotypic differences between mutant and wild-type IDH1/2 gliomas, the most salient is that IDH1/2 mutant glioma patients demonstrate markedly improved survival compared with IDH1/2 wild-type glioma patients. To address the mechanism underlying the superior clinical outcome of IDH1/2 mutant glioma patients, we investigated whether overexpression of the IDH1(R132H) protein could affect response to therapy in the context of an isogenic glioma cell background. Stable clonal U87MG and U373MG cell lines overexpressing IDH1(WT) and IDH1(R132H) were generated, as well as U87MG cell lines overexpressing IDH2(WT) and IDH2(R172K). In vitro experiments were conducted to characterize baseline growth and migration and response to radiation and temozolomide. In addition, reactive oxygen species (ROS) levels were measured under various conditions. U87MG-IDH1(R132H) cells, U373MG-IDH1(R132H) cells, and U87MG-IDH2(R172K) cells demonstrated increased sensitivity to radiation but not to temozolomide. Radiosensitization of U87MG-IDH1(R132H) cells was accompanied by increased apoptosis and accentuated ROS generation, and this effect was abrogated by the presence of the ROS scavenger N-acetyl-cysteine. Interestingly, U87MG-IDH1(R132H) cells also displayed decreased growth at higher cell density and in soft agar, as well as decreased migration. Overexpression of IDH1(R132H) and IDH2(R172K) mutant protein in glioblastoma cells resulted in increased radiation sensitivity and altered ROS metabolism and suppression of growth and migration in vitro. These findings provide insight into possible mechanisms contributing to the improved outcomes observed in patients with IDH1/2 mutant gliomas. 10.1093/neuonc/nos261
    Case-control study of the association between malignant brain tumours diagnosed between 2007 and 2009 and mobile and cordless phone use. Hardell Lennart,Carlberg Michael,Söderqvist Fredrik,Mild Kjell Hansson International journal of oncology Previous studies have shown a consistent association between long-term use of mobile and cordless phones and glioma and acoustic neuroma, but not for meningioma. When used these phones emit radiofrequency electromagnetic fields (RF-EMFs) and the brain is the main target organ for the handheld phone. The International Agency for Research on Cancer (IARC) classified in May, 2011 RF-EMF as a group 2B, i.e. a 'possible' human carcinogen. The aim of this study was to further explore the relationship between especially long-term (>10 years) use of wireless phones and the development of malignant brain tumours. We conducted a new case-control study of brain tumour cases of both genders aged 18-75 years and diagnosed during 2007-2009. One population-based control matched on gender and age (within 5 years) was used to each case. Here, we report on malignant cases including all available controls. Exposures on e.g. use of mobile phones and cordless phones were assessed by a self-administered questionnaire. Unconditional logistic regression analysis was performed, adjusting for age, gender, year of diagnosis and socio-economic index using the whole control sample. Of the cases with a malignant brain tumour, 87% (n=593) participated, and 85% (n=1,368) of controls in the whole study answered the questionnaire. The odds ratio (OR) for mobile phone use of the analogue type was 1.8, 95% confidence interval (CI)=1.04‑3.3, increasing with >25 years of latency (time since first exposure) to an OR=3.3, 95% CI=1.6-6.9. Digital 2G mobile phone use rendered an OR=1.6, 95% CI=0.996-2.7, increasing with latency >15-20 years to an OR=2.1, 95% CI=1.2-3.6. The results for cordless phone use were OR=1.7, 95% CI=1.1-2.9, and, for latency of 15-20 years, the OR=2.1, 95% CI=1.2-3.8. Few participants had used a cordless phone for >20-25 years. Digital type of wireless phones (2G and 3G mobile phones, cordless phones) gave increased risk with latency >1-5 years, then a lower risk in the following latency groups, but again increasing risk with latency >15-20 years. Ipsilateral use resulted in a higher risk than contralateral mobile and cordless phone use. Higher ORs were calculated for tumours in the temporal and overlapping lobes. Using the meningioma cases in the same study as reference entity gave somewhat higher ORs indicating that the results were unlikely to be explained by recall or observational bias. This study confirmed previous results of an association between mobile and cordless phone use and malignant brain tumours. These findings provide support for the hypothesis that RF-EMFs play a role both in the initiation and promotion stages of carcinogenesis. 10.3892/ijo.2013.2111
    Mobile phone use and incidence of glioma in the Nordic countries 1979-2008: consistency check. Deltour Isabelle,Auvinen Anssi,Feychting Maria,Johansen Christoffer,Klaeboe Lars,Sankila Risto,Schüz Joachim Epidemiology (Cambridge, Mass.) BACKGROUND:Some case-control studies have reported increased risks of glioma associated with mobile phone use. If true, this would ultimately affect the time trends for incidence rates (IRs). Correspondingly, lack of change in IRs would exclude certain magnitudes of risk. We investigated glioma IR trends in the Nordic countries, and compared the observed with expected incidence rates under various risk scenarios. METHODS:We analyzed annual age-standardized incidence rates in men and women aged 20 to 79 years during 1979-2008 using joinpoint regression (35,250 glioma cases). Probabilities of detecting various levels of relative risk were computed using simulations. RESULTS:For the period 1979 through 2008, the annual percent change in incidence rates was 0.4% (95% confidence interval = 0.1% to 0.6%) among men and 0.3% (0.1% to 0.5%) among women. Incidence rates have decreased in young men (20-39 years) since 1987, remained stable in middle-aged men (40-59 years) throughout the 30-year study period, and increased slightly in older men (60-79 years). In simulations, assumed relative risks for all users of 2.0 for an induction time of up to 15 years, 1.5 for up to 10 years, and 1.2 for up to 5 years were incompatible with observed incidence time trends. For heavy users of mobile phones, risks of 2.0 for up to 5 years' induction were also incompatible. CONCLUSION:No clear trend change in glioma incidence rates was observed. Several of the risk increases seen in case-control studies appear to be incompatible with the observed lack of incidence rate increase in middle-aged men. This suggests longer induction periods than currently investigated, lower risks than reported from some case-control studies, or the absence of any association. 10.1097/EDE.0b013e3182448295
    Epidemiology of gliomas. Ostrom Quinn T,Gittleman Haley,Stetson Lindsay,Virk Selene M,Barnholtz-Sloan Jill S Cancer treatment and research Gliomas are the most common type of primary intracranial tumors. Some glioma subtypes cause significant mortality and morbidity that are disproportionate to their relatively rare incidence. A very small proportion of glioma cases can be attributed to inherited genetic disorders. Many potential risk factors for glioma have been studied to date, but few provide explanation for the number of brain tumors identified. The most significant of these factors includes increased risk due to exposure to ionizing radiation, and decreased risk with history of allergy or atopic disease. The potential effect of exposure to cellular phones has been studied extensively, but the results remain inconclusive. Recent genomic analyses, using the genome-wide association study (GWAS) design, have identified several inherited risk variants that are associated with increased glioma risk. The following chapter provides an overview of the current state of research in the epidemiology of intracranial glioma. 10.1007/978-3-319-12048-5_1
    A forecasting method to reduce estimation bias in self-reported cell phone data. Redmayne Mary,Smith Euan,Abramson Michael J Journal of exposure science & environmental epidemiology There is ongoing concern that extended exposure to cell phone electromagnetic radiation could be related to an increased risk of negative health effects. Epidemiological studies seek to assess this risk, usually relying on participants' recalled use, but recall is notoriously poor. Our objectives were primarily to produce a forecast method, for use by such studies, to reduce estimation bias in the recalled extent of cell phone use. The method we developed, using Bayes' rule, is modelled with data we collected in a cross-sectional cluster survey exploring cell phone user-habits among New Zealand adolescents. Participants recalled their recent extent of SMS-texting and retrieved from their provider the current month's actual use-to-date. Actual use was taken as the gold standard in the analyses. Estimation bias arose from a large random error, as observed in all cell phone validation studies. We demonstrate that this seriously exaggerates upper-end forecasts of use when used in regression models. This means that calculations using a regression model will lead to underestimation of heavy-users' relative risk. Our Bayesian method substantially reduces estimation bias. In cases where other studies' data conforms to our method's requirements, application should reduce estimation bias, leading to a more accurate relative risk calculation for mid-to-heavy users. 10.1038/jes.2012.70
    Radiation-induced gliomas: a comprehensive review and meta-analysis. Yamanaka Ryuya,Hayano Azusa,Kanayama Tomohiko Neurosurgical review By conducting a systemic search of the PubMed database, we performed a comprehensive literature review to characterize secondary gliomas following radiotherapy treatment and to determine the most appropriate treatment strategy. Our analysis included 296 cases of radiation-induced gliomas. The primary lesion was characterized as a hematological malignancy in 104 cases (35.1 %), pituitary adenoma in 35 (11.8 %), craniopharyngioma in 19 (6.4 %), medulloblastoma in 38 (12.8 %), germ cell tumor in 13 (4.3 %), low-grade glioma in 28 (9.4 %), cancer/sarcoma in 12 (4.0 %), scalp region disease in 15 (5.0 %), meningioma/schwannoma in 13 (4.3 %), metastatic brain tumor in 5 (1.6 %), and other types (e.g., arteriovenous malformations and angiomas) in 14 (4.7 %). The average age of onset for primary lesions was 16.0 ± 15.8 years, and the average radiation dose delivered to the primary lesion was 37.6 ± 20.0 Gy. Secondary gliomas could be divided into grade I (1), grade II (32), grade III (88), and grade IV (173) tumors. The median overall survival for all glioma cases was 11 months (95 % confidence interval [CI], 9-12), with a 2-year survival rate of 20.2 %. On multivariate analysis, combined modality treatment and the latency period from the radiotherapy treatment to the glioma diagnosis were variables associated with the overall survival of patients with grade III/IV secondary gliomas. For patients treated with cranial radiotherapy, the risk of secondary glioma incidence warrants a longer follow-up period beyond the standard time frame typically designated for determining the risk of primary tumor relapse. Moreover, combination therapy is a potential treatment option for radiation-induced gliomas. 10.1007/s10143-016-0786-8
    Mobile phones, brain tumors, and the interphone study: where are we now? Swerdlow Anthony J,Feychting Maria,Green Adele C,Leeka Kheifets Leeka Kheifets,Savitz David A, Environmental health perspectives BACKGROUND:In the past 15 years, mobile telephone use has evolved from an uncommon activity to one with > 4.6 billion subscriptions worldwide. However, there is public concern about the possibility that mobile phones might cause cancer, especially brain tumors. OBJECTIVES:We reviewed the evidence on whether mobile phone use raises the risk of the main types of brain tumor—glioma and meningioma—with a particular focus on the recent publication of the largest epidemiologic study yet: the 13-country Interphone Study. DISCUSSION:Methodological defcits limit the conclusions that can be drawn from the Interphone study, but its results, along with those from other epidemiologic, biological, and animal studies and brain tumor incidence trends, suggest that within about 10–15 years after first use of mobile phones there is unlikely to be a material increase in the risk of brain tumors in adults. Data for childhood tumors and for periods beyond 15 years are currently lacking. CONCLUSIONS:Although there remains some uncertainty, the trend in the accumulating evidence is increasingly against the hypothesis that mobile phone use can cause brain tumors in adults. 10.1289/ehp.1103693
    The controversy about a possible relationship between mobile phone use and cancer. Kundi Michael Environmental health perspectives OBJECTIVE:During the last decade, mobile phone use increased to almost 100% prevalence in many countries of the world. Evidence for potential health hazards accumulated in parallel by epidemiologic investigations has raised controversies about the appropriate interpretation and the degree of bias and confounding responsible for reduced or increased risk estimates. DATA SOURCES:Overall, I identified 33 epidemiologic studies in the peer-reviewed literature, most of which (25) were about brain tumors. Two groups have collected data for >or=10 years of mobile phone use: Hardell and colleagues from Sweden and the Interphone group, an international consortium from 13 countries coordinated by the International Agency for Research on Cancer. DATA SYNTHESIS:Combined odds ratios (95% confidence intervals) from these studies for glioma, acoustic neuroma, and meningioma were 1.5 (1.2-1.8); 1.3 (0.95-1.9); and 1.1 (0.8-1.4), respectively. CONCLUSIONS:Methodologic considerations revealed that three important conditions for epidemiologic studies to detect an increased risk are not met: a ) no evidence-based exposure metric is available; b) the observed duration of mobile phone use is generally still too low; c) no evidence-based selection of end points among the grossly different types of neoplasias is possible because of lack of etiologic hypotheses. Concerning risk estimates, selection bias, misclassification bias, and effects of the disease on mobile phone use could have reduced estimates, and recall bias may have led to spuriously increased risks. The overall evidence speaks in favor of an increased risk, but its magnitude cannot be assessed at present because of insufficient information on long-term use. 10.1289/ehp.11902
    Mobile phone use and location of glioma: a case-case analysis. Hartikka Hanna,Heinävaara Sirpa,Mäntylä Riitta,Kähärä Veikko,Kurttio Päivi,Auvinen Anssi Bioelectromagnetics We assessed a new approach for evaluating the glioma risk among users of mobile phones to focus on the part of the brain most heavily exposed to radiofrequency electromagnetic fields from mobile phones. The tumor midpoint was defined from radiological imaging. A case-case analysis with 99 gliomas was performed using logistic regression. The exposed cases were those with the tumor mid-point within 4.6 cm from the line between the mouth and the external meatus of the ear, representing the most likely location of the mobile phone (the source of exposure). Alternative analyses based on various indicators of mobile phone use as the outcome were also carried out. The majority of cases were regular mobile phone users. A slightly higher proportion of gliomas among mobile phone users than non-users occurred within 4.6 cm from the presumed location of the mobile phone (28% vs. 14%). Modestly elevated odds ratios were observed for several indicators of mobile phone use, but without an exposure gradient. The highest odds ratios were found for contralateral and short-term use. Our results, though limited by the small sample size, demonstrate that detailed information on tumor location allows evaluation of the risk related to the most heavily exposed part of the brain, representing direct evaluation of the possible local carcinogenic effects of the radiofrequency fields. However, field strength varies between users and over time also within a given anatomic site, due to the output power of the phone. Collaborative analysis of a larger sample is planned. 10.1002/bem.20471
    Epidemiological evidence for an association between use of wireless phones and tumor diseases. Hardell Lennart,Carlberg Michael,Hansson Mild Kjell Pathophysiology : the official journal of the International Society for Pathophysiology During recent years there has been increasing public concern on potential cancer risks from microwave emissions from wireless phones. We evaluated the scientific evidence for long-term mobile phone use and the association with certain tumors in case-control studies, mostly from the Hardell group in Sweden and the Interphone study group. Regarding brain tumors the meta-analysis yielded for glioma odds ratio (OR)=1.0, 95% confidence interval (CI)=0.9-1.1. OR increased to 1.3, 95% CI=1.1-1.6 with 10 year latency period, with highest risk for ipsilateral exposure (same side as the tumor localisation), OR=1.9, 95% CI=1.4-2.4, lower for contralateral exposure (opposite side) OR=1.2, 95% CI=0.9-1.7. Regarding acoustic neuroma OR=1.0, 95% CI=0.8-1.1 was calculated increasing to OR=1.3, 95% CI=0.97-1.9 with 10 year latency period. For ipsilateral exposure OR=1.6, 95% CI=1.1-2.4, and for contralateral exposure OR=1.2, 95% CI=0.8-1.9 were found. Regarding meningioma no consistent pattern of an increased risk was found. Concerning age, highest risk was found in the age group <20 years at time of first use of wireless phones in the studies from the Hardell group. For salivary gland tumors, non-Hodgkin lymphoma and testicular cancer no consistent pattern of an association with use of wireless phones was found. One study on uveal melanoma yielded for probable/certain mobile phone use OR=4.2, 95% CI=1.2-14.5. One study on intratemporal facial nerve tumor was not possible to evaluate due to methodological shortcomings. In summary our review yielded a consistent pattern of an increased risk for glioma and acoustic neuroma after >10 year mobile phone use. We conclude that current standard for exposure to microwaves during mobile phone use is not safe for long-term exposure and needs to be revised. 10.1016/j.pathophys.2009.01.003
    The epidemiology of glioma in adults: a "state of the science" review. Ostrom Quinn T,Bauchet Luc,Davis Faith G,Deltour Isabelle,Fisher James L,Langer Chelsea Eastman,Pekmezci Melike,Schwartzbaum Judith A,Turner Michelle C,Walsh Kyle M,Wrensch Margaret R,Barnholtz-Sloan Jill S Neuro-oncology Gliomas are the most common primary intracranial tumor, representing 81% of malignant brain tumors. Although relatively rare, they cause significant mortality and morbidity. Glioblastoma, the most common glioma histology (∼45% of all gliomas), has a 5-year relative survival of ∼5%. A small portion of these tumors are caused by Mendelian disorders, including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome. Genomic analyses of glioma have also produced new evidence about risk and prognosis. Recently discovered biomarkers that indicate improved survival include O⁶-methylguanine-DNA methyltransferase methylation, isocitrate dehydrogenase mutation, and a glioma cytosine-phosphate-guanine island methylator phenotype. Genome-wide association studies have identified heritable risk alleles within 7 genes that are associated with increased risk of glioma. Many risk factors have been examined as potential contributors to glioma risk. Most significantly, these include an increase in risk by exposure to ionizing radiation and a decrease in risk by history of allergies or atopic disease(s). The potential influence of occupational exposures and cellular phones has also been examined, with inconclusive results. We provide a “state of the science” review of current research into causes and risk factors for gliomas in adults. 10.1093/neuonc/nou087
    Medical diagnostic radiation exposures and risk of gliomas. Davis Faith,Il'yasova Dora,Rankin Kristin,McCarthy Bridget,Bigner Darell D Radiation research High-dose ionizing radiation is an established risk factor for glioma, but it remains unknown whether moderate- and low-dose radiation increase glioma risk. In this analysis, we assessed the evidence that self-reported exposures to diagnostic ionizing radiation, including computerized tomography (CT) scans, is associated with increased risk of adult glioma. While no independent association was observed for CT scans alone (3+ scans compared to none P = 0.08 and 1-2 scans compared to none P = 0.68), our findings suggest an increased risk of adult gliomas with cumulative exposure to three or more CT scans to the head and neck region (OR = 1.97, 95% CI: 0.92-4.23) limited to those who reported a family history of cancer: the P value for the interaction between having three or more CT scans and family history of cancer was 0.08. The stratum-specific adjusted OR for those with family history of cancer was more than three times that for the sub-group without family history of cancer. While there is some potential for symptom-related bias, one might expect this to be present for all diagnostic procedures rather than specific to one procedure. The interaction between CT scans and glioma with family history of cancer supports the biological plausibility of our findings, because similar results have been found for breast cancer and radiation. This observational data will increase awareness about potential risks associated with CT scans and the need to minimize the use of unnecessary examinations. 10.1667/RR2186.1
    Time trends in brain tumor incidence rates in Denmark, Finland, Norway, and Sweden, 1974-2003. Deltour Isabelle,Johansen Christoffer,Auvinen Anssi,Feychting Maria,Klaeboe Lars,Schüz Joachim Journal of the National Cancer Institute In Denmark, Finland, Norway, and Sweden, the use of mobile phones increased sharply in the mid-1990s; thus, time trends in brain tumor incidence after 1998 may provide information about possible tumor risks associated with mobile phone use. We investigated time trends in the incidence of glioma and meningioma in Denmark, Finland, Norway, and Sweden from 1974 to 2003, using data from national cancer registries. We used joinpoint regression models to analyze the annual incidence rates of glioma and meningioma. During this period, 59,984 men and women aged 20-79 years were diagnosed with brain tumors in a population of 16 million adults. All statistical tests were two-sided. From 1974 to 2003, the incidence rate of glioma increased by 0.5% per year (95% confidence interval [CI] = 0.2% to 0.8%) among men and by 0.2% per year (95% CI = -0.1% to 0.5%) among women and that of meningioma increased by 0.8% per year (95% CI = 0.4% to 1.3%) among men, and after the early 1990s, by 3.8% per year (95% CI = 3.2% to 4.4%) among women. No change in incidence trends were observed from 1998 to 2003, the time when possible associations between mobile phone use and cancer risk would be informative about an induction period of 5-10 years. 10.1093/jnci/djp415
    Use of mobile phones and cordless phones is associated with increased risk for glioma and acoustic neuroma. Hardell Lennart,Carlberg Michael,Hansson Mild Kjell Pathophysiology : the official journal of the International Society for Pathophysiology The International Agency for Research on Cancer (IARC) at WHO evaluation of the carcinogenic effect of RF-EMF on humans took place during a 24-31 May 2011 meeting at Lyon in France. The Working Group consisted of 30 scientists and categorised the radiofrequency electromagnetic fields from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields (RF-EMF), as Group 2B, i.e., a 'possible', human carcinogen. The decision on mobile phones was based mainly on the Hardell group of studies from Sweden and the IARC Interphone study. We give an overview of current epidemiological evidence for an increased risk for brain tumours including a meta-analysis of the Hardell group and Interphone results for mobile phone use. Results for cordless phones are lacking in Interphone. The meta-analysis gave for glioma in the most exposed part of the brain, the temporal lobe, odds ratio (OR)=1.71, 95% confidence interval (CI)=1.04-2.81 in the ≥10 years (>10 years in the Hardell group) latency group. Ipsilateral mobile phone use ≥1640h in total gave OR=2.29, 95% CI=1.56-3.37. The results for meningioma were OR=1.25, 95% CI=0.31-4.98 and OR=1.35, 95% CI=0.81-2.23, respectively. Regarding acoustic neuroma ipsilateral mobile phone use in the latency group ≥10 years gave OR=1.81, 95% CI=0.73-4.45. For ipsilateral cumulative use ≥1640h OR=2.55, 95% CI=1.50-4.40 was obtained. Also use of cordless phones increased the risk for glioma and acoustic neuroma in the Hardell group studies. Survival of patients with glioma was analysed in the Hardell group studies yielding in the >10 years latency period hazard ratio (HR)=1.2, 95% CI=1.002-1.5 for use of wireless phones. This increased HR was based on results for astrocytoma WHO grade IV (glioblastoma multiforme). Decreased HR was found for low-grade astrocytoma, WHO grades I-II, which might be caused by RF-EMF exposure leading to tumour-associated symptoms and earlier detection and surgery with better prognosis. Some studies show increasing incidence of brain tumours whereas other studies do not. It is concluded that one should be careful using incidence data to dismiss results in analytical epidemiology. The IARC carcinogenic classification does not seem to have had any significant impact on governments' perceptions of their responsibilities to protect public health from this widespread source of radiation. 10.1016/j.pathophys.2012.11.001
    Inferring the 1985-2014 impact of mobile phone use on selected brain cancer subtypes using Bayesian structural time series and synthetic controls. de Vocht Frank Environment international BACKGROUND:Mobile phone use has been increasing rapidly in the past decades and, in parallel, so has the annual incidence of certain types of brain cancers. However, it remains unclear whether this correlation is coincidental or whether use of mobile phones may cause the development, promotion or progression of specific cancers. The 1985-2014 incidence of selected brain cancer subtypes in England were analyzed and compared to counterfactual 'synthetic control' timeseries. METHODS:Annual 1985-2014 incidence of malignant glioma, glioblastoma multiforme, and malignant neoplasms of the temporal and parietal lobes in England were modelled based on population-level covariates using Bayesian structural time series models assuming 5,10 and 15year minimal latency periods. Post-latency counterfactual 'synthetic England' timeseries were nowcast based on covariate trends. The impact of mobile phone use was inferred from differences between measured and modelled time series. RESULTS:There is no evidence of an increase in malignant glioma, glioblastoma multiforme, or malignant neoplasms of the parietal lobe not predicted in the 'synthetic England' time series. Malignant neoplasms of the temporal lobe however, have increased faster than expected. A latency period of 10years reflected the earliest latency period when this was measurable and related to mobile phone penetration rates, and indicated an additional increase of 35% (95% Credible Interval 9%:59%) during 2005-2014; corresponding to an additional 188 (95%CI 48-324) cases annually. CONCLUSIONS:A causal factor, of which mobile phone use (and possibly other wireless equipment) is in agreement with the hypothesized temporal association, is related to an increased risk of developing malignant neoplasms in the temporal lobe. 10.1016/j.envint.2016.10.019
    Mobile phone use and risk of intracranial tumors: a consistency analysis. Lagorio Susanna,Röösli Martin Bioelectromagnetics A meta-analysis of studies on intracranial tumors and mobile phone use published by the end of 2012 was performed to evaluate the overall consistency of findings, assess the sensitivity of results to changes in the dataset, and try to detect the sources of between-study heterogeneity. Twenty-nine papers met our inclusion criteria. These papers reported on 47 eligible studies (17 on glioma, 15 on meningioma, 15 on acoustic neuroma), consisting of either primary investigations or pooled analyses. Five combinations of non-overlapping studies per outcome were identified. The combined relative risks (cRRs) in long-term mobile phone users (≥10 years) ranged between 0.98 (0.75-1.28) and 1.11 (0.86-1.44) for meningioma, with little heterogeneity across studies. High heterogeneity was detected across estimates of glioma and acoustic neuroma risk in long term users, with cRRs ranging between 1.19 (95% CI 0.86-1.64) and 1.40 (0.96-2.04), and from 1.14 (0.65-1.99) to 1.33 (0.65-2.73), respectively. A meta-regression of primary studies showed that the methodological differences embedded in the variable "study-group" explained most of the overall heterogeneity in results. Summary risk estimates based on heterogeneous findings should not be over-interpreted. Overall, the results of our study detract from the hypothesis that mobile phone use affects the occurrence of intracranial tumors. However, reproducibility (or lack of) is just one clue in the critical appraisal of epidemiological evidence. Based on other considerations, such as the limited knowledge currently available on risk beyond 15 years from first exposure, or following mobile phone use started in childhood, the pursuance of epidemiological surveillance is warranted. 10.1002/bem.21829
    Long-term use of cellular phones and brain tumours: increased risk associated with use for > or =10 years. Hardell Lennart,Carlberg Michael,Söderqvist Fredrik,Mild Kjell Hansson,Morgan L Lloyd Occupational and environmental medicine AIM:To evaluate brain tumour risk among long-term users of cellular telephones. METHODS:Two cohort studies and 16 case-control studies on this topic were identified. Data were scrutinised for use of mobile phone for > or =10 years and ipsilateral exposure if presented. RESULTS:The cohort study was of limited value due to methodological shortcomings in the study. Of the 16 case-control studies, 11 gave results for > or =10 years' use or latency period. Most of these results were based on low numbers. An association with acoustic neuroma was found in four studies in the group with at least 10 years' use of a mobile phone. No risk was found in one study, but the tumour size was significantly larger among users. Six studies gave results for malignant brain tumours in that latency group. All gave increased odd ratios (OR), especially for ipsilateral exposure. In a meta-analysis, ipsilateral cell phone use for acoustic neuroma was OR = 2.4 (95% CI 1.1 to 5.3) and OR = 2.0, (1.2 to 3.4) for glioma using a tumour latency period of > or =10 years. CONCLUSIONS:Results from present studies on use of mobile phones for > or =10 years give a consistent pattern of increased risk for acoustic neuroma and glioma. The risk is highest for ipsilateral exposure. 10.1136/oem.2006.029751
    Swedish review strengthens grounds for concluding that radiation from cellular and cordless phones is a probable human carcinogen. Davis Devra Lee,Kesari Santosh,Soskolne Colin L,Miller Anthony B,Stein Yael Pathophysiology : the official journal of the International Society for Pathophysiology With 5.9 billion reported users, mobile phones constitute a new, ubiquitous and rapidly growing exposure worldwide. Mobile phones are two-way microwave radios that also emit low levels of electromagnetic radiation. Inconsistent results have been published on potential risks of brain tumors tied with mobile phone use as a result of important methodological differences in study design and statistical power. Some studies have examined mobile phone users for periods of time that are too short to detect an increased risk of brain cancer, while others have misclassified exposures by placing those with exposures to microwave radiation from cordless phones in the control group, or failing to attribute such exposures in the cases. In 2011, the World Health Organization, International Agency for Research on Cancer (IARC) advised that electromagnetic radiation from mobile phone and other wireless devices constitutes a "possible human carcinogen," 2B. Recent analyses not considered in the IARC review that take into account these methodological shortcomings from a number of authors find that brain tumor risk is significantly elevated for those who have used mobile phones for at least a decade. Studies carried out in Sweden indicate that those who begin using either cordless or mobile phones regularly before age 20 have greater than a fourfold increased risk of ipsilateral glioma. Given that treatment for a single case of brain cancer can cost between $100,000 for radiation therapy alone and up to $1 million depending on drug costs, resources to address this illness are already in short supply and not universally available in either developing or developed countries. Significant additional shortages in oncology services are expected at the current growth of cancer. No other environmental carcinogen has produced evidence of an increased risk in just one decade. Empirical data have shown a difference in the dielectric properties of tissues as a function of age, mostly due to the higher water content in children's tissues. High resolution computerized models based on human imaging data suggest that children are indeed more susceptible to the effects of EMF exposure at microwave frequencies. If the increased brain cancer risk found in young users in these recent studies does apply at the global level, the gap between supply and demand for oncology services will continue to widen. Many nations, phone manufacturers, and expert groups, advise prevention in light of these concerns by taking the simple precaution of "distance" to minimize exposures to the brain and body. We note than brain cancer is the proverbial "tip of the iceberg"; the rest of the body is also showing effects other than cancers. 10.1016/j.pathophys.2013.03.001
    The INTERPHONE study: design, epidemiological methods, and description of the study population. Cardis Elisabeth,Richardson Lesley,Deltour Isabelle,Armstrong Bruce,Feychting Maria,Johansen Christoffer,Kilkenny Monique,McKinney Patricia,Modan Baruch,Sadetzki Siegal,Schüz Joachim,Swerdlow Anthony,Vrijheid Martine,Auvinen Anssi,Berg Gabriele,Blettner Maria,Bowman Joseph,Brown Julianne,Chetrit Angela,Christensen Helle Collatz,Cook Angus,Hepworth Sarah,Giles Graham,Hours Martine,Iavarone Ivano,Jarus-Hakak Avital,Klaeboe Lars,Krewski Daniel,Lagorio Susanna,Lönn Stefan,Mann Simon,McBride Mary,Muir Kenneth,Nadon Louise,Parent Marie-Elise,Pearce Neil,Salminen Tiina,Schoemaker Minouk,Schlehofer Brigitte,Siemiatycki Jack,Taki Masao,Takebayashi Toru,Tynes Tore,van Tongeren Martie,Vecchia Paolo,Wiart Joe,Woodward Alistair,Yamaguchi Naohito European journal of epidemiology The very rapid worldwide increase in mobile phone use in the last decade has generated considerable interest in the possible health effects of exposure to radio frequency (RF) fields. A multinational case-control study, INTERPHONE, was set-up to investigate whether mobile phone use increases the risk of cancer and, more specifically, whether the RF fields emitted by mobile phones are carcinogenic. The study focused on tumours arising in the tissues most exposed to RF fields from mobile phones: glioma, meningioma, acoustic neurinoma and parotid gland tumours. In addition to a detailed history of mobile phone use, information was collected on a number of known and potential risk factors for these tumours. The study was conducted in 13 countries. Australia, Canada, Denmark, Finland, France, Germany, Israel, Italy, Japan, New Zealand, Norway, Sweden, and the UK using a common core protocol. This paper describes the study design and methods and the main characteristics of the study population. INTERPHONE is the largest case-control study to date investigating risks related to mobile phone use and to other potential risk factors for the tumours of interest and includes 2,765 glioma, 2,425 meningioma, 1,121 acoustic neurinoma, 109 malignant parotid gland tumour cases and 7,658 controls. Particular attention was paid to estimating the amount and direction of potential recall and participation biases and their impact on the study results. 10.1007/s10654-007-9152-z
    Mobile phone radiation causes brain tumors and should be classified as a probable human carcinogen (2A) (review). Morgan L Lloyd,Miller Anthony B,Sasco Annie,Davis Devra Lee International journal of oncology Quickly changing technologies and intensive uses of radiofrequency electromagnetic field (RF-EMF)‑emitting phones pose a challenge to public health. Mobile phone users and uses and exposures to other wireless transmitting devices (WTDs) have increased in the past few years. We consider that CERENAT, a French national study, provides an important addition to the literature evaluating the use of mobile phones and risk of brain tumors. The CERENAT finding of increased risk of glioma is consistent with studies that evaluated use of mobile phones for a decade or longer and corroborate those that have shown a risk of meningioma from mobile phone use. In CERENAT, exposure to RF‑EMF from digitally enhanced cordless telephones (DECTs), used by over half the population of France during the period of this study, was not evaluated. If exposures to DECT phones could have been taken into account, the risks of glioma from mobile phone use in CERENAT are likely to be higher than published. We conclude that radiofrequency fields should be classified as a Group 2A ̔probable̓ human carcinogen under the criteria used by the International Agency for Research on Cancer (Lyon, France). Additional data should be gathered on exposures to mobile and cordless phones, other WTDs, mobile phone base stations and Wi‑Fi routers to evaluate their impact on public health. We advise that the as low as reasonable achievable (ALARA) principle be adopted for uses of this technology, while a major cross‑disciplinary effort is generated to train researchers in bioelectromagnetics and provide monitoring of potential health impacts of RF‑EMF. 10.3892/ijo.2015.2908
    Occurrence of primary brain tumors in cochlear implant patients in Sweden between 1989 and 2014. Smeds Henrik,Wales Jeremy,Mathiesen Tiit,Talbäck Mats,Feychting Maria Clinical epidemiology Purpose:Cochlear implants are widely used for hearing rehabilitation of deaf children with congenital deafness or adults with acquired severe-to-profound hearing loss. The sound processor antenna creates a radio frequency-electromagnetic field transmitting the sound signal to the implant, similar to that in a mobile phone. A recent case report suggested a relationship between cochlear implants and malignant glioma, and some epidemiological studies have suggested an increased glioma and acoustic neuroma risk associated with long hours of mobile phone use. An epidemiological study is warranted to evaluate such a relationship in patients with cochlear implants. Patients and methods:To examine whether this chronic radio frequency-electromagnetic field signaling is associated with an increased brain tumor risk, a population-based cohort study was performed examining all 2,748 patients receiving a cochlear implant in Sweden during the years 1989-2014. In all, 3,169 surgeries were performed in the total cohort. The expected occurrence of glioma, meningioma, and acoustic neuroma in the patient cohort was calculated using specific national incidence rates in the Swedish population. Results:Four patients were diagnosed with a brain tumor during follow-up, three of them having meningioma compared with 0.95 expected (standardized incidence ratio =3.16, 95% CI 0.65-9.24), and one had glioma compared with 1.34 expected (standardized incidence ratio =0.75, 95% CI 0.02-4.15). No case of acoustic neuroma was observed compared with 0.09 expected. Conclusion:In this study, we did not find support for concerns raised in a previous case report regarding a potentially higher risk of glioma. The number of brain tumors observed was well within the numbers expected from national incidence figures. Although this was a relatively small cohort with a limited follow-up time, it is the largest epidemiological study to date to address this concern. 10.2147/CLEP.S164556
    Cell phones and brain tumors: a review including the long-term epidemiologic data. Khurana Vini G,Teo Charles,Kundi Michael,Hardell Lennart,Carlberg Michael Surgical neurology BACKGROUND:The debate regarding the health effects of low-intensity electromagnetic radiation from sources such as power lines, base stations, and cell phones has recently been reignited. In the present review, the authors attempt to address the following question: is there epidemiologic evidence for an association between long-term cell phone usage and the risk of developing a brain tumor? Included with this meta-analysis of the long-term epidemiologic data are a brief overview of cell phone technology and discussion of laboratory data, biological mechanisms, and brain tumor incidence. METHODS:In order to be included in the present meta-analysis, studies were required to have met all of the following criteria: (i) publication in a peer-reviewed journal; (ii) inclusion of participants using cell phones for > or = 10 years (ie, minimum 10-year "latency"); and (iii) incorporation of a "laterality" analysis of long-term users (ie, analysis of the side of the brain tumor relative to the side of the head preferred for cell phone usage). This is a meta-analysis incorporating all 11 long-term epidemiologic studies in this field. RESULTS:The results indicate that using a cell phone for > or = 10 years approximately doubles the risk of being diagnosed with a brain tumor on the same ("ipsilateral") side of the head as that preferred for cell phone use. The data achieve statistical significance for glioma and acoustic neuroma but not for meningioma. CONCLUSION:The authors conclude that there is adequate epidemiologic evidence to suggest a link between prolonged cell phone usage and the development of an ipsilateral brain tumor. 10.1016/j.surneu.2009.01.019
    Epidemiology of primary brain tumors: current concepts and review of the literature. Wrensch Margaret,Minn Yuriko,Chew Terri,Bondy Melissa,Berger Mitchel S Neuro-oncology The purpose of this review is to provide a sufficiently detailed perspective on epidemiologic studies of primary brain tumors to encourage multidisciplinary etiologic and prognostic studies among surgeons, neuro-oncologists, epidemiologists, and molecular scientists. Molecular tumor markers that predict survival and treatment response are being identified with hope of even greater gains in this area from emerging array technologies. Regarding risk factors, studies of inherited susceptibility and constitutive polymorphisms in genes pertinent to carcinogenesis (for example, DNA repair and detoxification genes and mutagen sensitivity) have revealed provocative findings. Inverse associations of the history of allergies with glioma risk observed in 3 large studies and reports of inverse associations of glioma with common infections suggest a possible role of immune factors in glioma genesis or progression. Studies continue to suggest that brain tumors might result from workplace, dietary, and other personal and residential exposures, but studies of cell phone use and power frequency electromagnetic fields have found little to support a causal connection with brain tumors; caveats remain. The only proven causes of brain tumors (that is, rare hereditary syndromes, therapeutic radiation, and immune suppression giving rise to brain lymphomas) account for a small proportion of cases. Progress in understanding primary brain tumors might result from studies of well-defined histologic and molecular tumor types incorporating assessment of potentially relevant information on subject susceptibility and environmental and noninherited endogenous factors (viruses, radiation, and carcinogenic or protective chemical exposures through diet, workplace, oxidative metabolism, or other sources). Such studies will require the cooperation of researchers from many disciplines. 10.1093/neuonc/4.4.278
    Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five Interphone countries. Cardis E,Armstrong B K,Bowman J D,Giles G G,Hours M,Krewski D,McBride M,Parent M E,Sadetzki S,Woodward A,Brown J,Chetrit A,Figuerola J,Hoffmann C,Jarus-Hakak A,Montestruq L,Nadon L,Richardson L,Villegas R,Vrijheid M Occupational and environmental medicine OBJECTIVES:The objective of this study was to examine the associations of brain tumours with radio frequency (RF) fields from mobile phones. METHODS:Patients with brain tumour from the Australian, Canadian, French, Israeli and New Zealand components of the Interphone Study, whose tumours were localised by neuroradiologists, were analysed. Controls were matched on age, sex and region and allocated the 'tumour location' of their matched case. Analyses included 553 glioma and 676 meningioma cases and 1762 and 1911 controls, respectively. RF dose was estimated as total cumulative specific energy (TCSE; J/kg) absorbed at the tumour's estimated centre taking into account multiple RF exposure determinants. RESULTS:ORs with ever having been a regular mobile phone user were 0.93 (95% CI 0.73 to 1.18) for glioma and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for glioma were below 1 in the first four quintiles of TCSE but above 1 in the highest quintile, 1.35 (95% CI 0.96 to 1.90). The OR increased with increasing TCSE 7+ years before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to 3.47 in the highest quintile). A complementary analysis in which 44 glioma and 135 meningioma cases in the most exposed area of the brain were compared with gliomas and meningiomas located elsewhere in the brain showed increased ORs for tumours in the most exposed part of the brain in those with 10+ years of mobile phone use (OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for meningioma were similar, but ORs were lower, many below 1.0. CONCLUSIONS:There were suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk. The uncertainty of these results requires that they be replicated before a causal interpretation can be made. 10.1136/oemed-2011-100155
    Mobile phone use and risk of brain neoplasms and other cancers: prospective study. Benson Victoria S,Pirie Kirstin,Schüz Joachim,Reeves Gillian K,Beral Valerie,Green Jane, International journal of epidemiology BACKGROUND:Results from some retrospective studies suggest a possible increased risk of glioma and acoustic neuroma in users of mobile phones. METHODS:The relation between mobile phone use and incidence of intracranial central nervous system (CNS) tumours and other cancers was examined in 791,710 middle-aged women in a UK prospective cohort, the Million Women Study. Cox regression models were used to estimate adjusted relative risks (RRs) and 95% confidence intervals (CIs). Women reported mobile phone use in 1999 to 2005 and again in 2009. RESULTS:During 7 years' follow-up, 51,680 incident invasive cancers and 1,261 incident intracranial CNS tumours occurred. Risk among ever vs never users of mobile phones was not increased for all intracranial CNS tumours (RR = 1.01, 95% CI = 0.90-1.14, P = 0.82), for specified CNS tumour types nor for cancer at 18 other specified sites. For long-term users compared with never users, there was no appreciable association for glioma (10+ years: RR = 0.78, 95% CI = 0.55-1.10, P = 0.16) or meningioma (10+ years: RR = 1.10, 95% CI = 0.66-1.84, P = 0.71). For acoustic neuroma, there was an increase in risk with long term use vs never use (10+ years: RR = 2.46, 95% CI = 1.07-5.64, P = 0.03), the risk increasing with duration of use (trend among users, P = 0.03). CONCLUSIONS:In this large prospective study, mobile phone use was not associated with increased incidence of glioma, meningioma or non-CNS cancers. 10.1093/ije/dyt072
    Medical exposure to ionising radiation and the risk of brain tumours: Interphone study group, Germany. Blettner Maria,Schlehofer Brigitte,Samkange-Zeeb Florence,Berg Gabriele,Schlaefer Klaus,Schüz Joachim European journal of cancer (Oxford, England : 1990) BACKGROUND:The role of exposure to low doses of ionising radiation in the aetiology of brain tumours has yet to be clarified. The objective of this study was to investigate the association between medically or occupationally related exposure to ionising radiation and brain tumours. METHODS:We used self-reported medical and occupational data collected during the German part of a multinational case-control study on mobile phone use and the risk of brain tumours (Interphone study) for the analyses. RESULTS:For any exposure to medical ionising radiation we found odds ratios (ORs) of 0.63 (95% confidence interval (CI)=0.48-0.83), 1.08 (95% CI=0.80-1.45) and 0.97 (95% CI=0.54-1.75) for glioma, meningioma and acoustic neuroma, respectively. Elevated ORs were found for meningioma (OR 2.32, 95% CI: 0.90-5.96) and acoustic neuroma (OR 6.45, 95% CI: 0.62-67.16) for radiotherapy to the head and neck regions. CONCLUSION:We did not find any significant increased risk of brain tumours for exposure to medical ionising radiation. 10.1016/j.ejca.2007.06.020
    Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. International journal of epidemiology BACKGROUND:The rapid increase in mobile telephone use has generated concern about possible health risks related to radiofrequency electromagnetic fields from this technology. METHODS:An interview-based case-control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol. RESULTS:A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70-0.94] and meningioma (OR 0.79; 95% CI 0.68-0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed > or =10 years after first phone use (glioma: OR 0.98; 95% CI 0.76-1.26; meningioma: OR 0.83; 95% CI 0.61-1.14). ORs were <1.0 for all deciles of lifetime number of phone calls and nine deciles of cumulative call time. In the 10th decile of recalled cumulative call time, > or =1640 h, the OR was 1.40 (95% CI 1.03-1.89) for glioma, and 1.15 (95% CI 0.81-1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma tended to be greater in subjects who reported usual phone use on the same side of the head as their tumour than on the opposite side. CONCLUSIONS:Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation. 10.1093/ije/dyq079
    Long-term mobile phone use and brain tumor risk. Lönn Stefan,Ahlbom Anders,Hall Per,Feychting Maria, American journal of epidemiology Handheld mobile phones were introduced in Sweden during the late 1980s. The purpose of this population-based, case-control study was to test the hypothesis that long-term mobile phone use increases the risk of brain tumors. The authors identified all cases aged 20-69 years who were diagnosed with glioma or meningioma during 2000-2002 in certain parts of Sweden. Randomly selected controls were stratified on age, gender, and residential area. Detailed information about mobile phone use was collected from 371 (74%) glioma and 273 (85%) meningioma cases and 674 (71%) controls. For regular mobile phone use, the odds ratio was 0.8 (95% confidence interval: 0.6, 1.0) for glioma and 0.7 (95% confidence interval: 0.5, 0.9) for meningioma. Similar results were found for more than 10 years' duration of mobile phone use. No risk increase was found for ipsilateral phone use for tumors located in the temporal and parietal lobes. Furthermore, the odds ratio did not increase, regardless of tumor histology, type of phone, and amount of use. This study includes a large number of long-term mobile phone users, and the authors conclude that the data do not support the hypothesis that mobile phone use is related to an increased risk of glioma or meningioma. 10.1093/aje/kwi091
    Occupational exposure to ionizing and non-ionizing radiation and risk of glioma. Hocking Bruce Occupational medicine (Oxford, England) 10.1093/occmed/kqm143
    Letter to the Editor Regarding "Wireless Phone Use and Risk of Adult Glioma: Evidence from a Meta-Analysis". Mortazavi Seyed Alireza,Mortazavi Seyed Mohammad Javad World neurosurgery 10.1016/j.wneu.2018.06.128
    Mobile phone radiation and the risk of cancer; a review. Abdus-salam A,Elumelu T,Adenipekun A African journal of medicine and medical sciences With the licensing of mobile phone operators about 7 years ago, Nigeria joined many countries where worries about the health risks (including carcinogenesis) of mobile phones have become common. Opinions have also been expressed by many, some of which were inaccurate in the light of scientific evidence. This article reviewed the current scientific evidence of the role of mobile phones as possible cancer risk. The preponderance of published research works over several decades including some with over ten years of follow up have not demonstrated any significant increase in cancer among mobile phone users. However, the need for caution is emphasized as it may take up to four decades for carcinogenesis to become fully apparent.
    Probabilistic Multiple-Bias Modeling Applied to the Canadian Data From the Interphone Study of Mobile Phone Use and Risk of Glioma, Meningioma, Acoustic Neuroma, and Parotid Gland Tumors. Momoli F,Siemiatycki J,McBride M L,Parent M-É,Richardson L,Bedard D,Platt R,Vrijheid M,Cardis E,Krewski D American journal of epidemiology We undertook a re-analysis of the Canadian data from the 13-country case-control Interphone Study (2001-2004), in which researchers evaluated the associations of mobile phone use with the risks of brain, acoustic neuroma, and parotid gland tumors. In the main publication of the multinational Interphone Study, investigators concluded that biases and errors prevented a causal interpretation. We applied a probabilistic multiple-bias model to address possible biases simultaneously, using validation data from billing records and nonparticipant questionnaires as information on recall error and selective participation. In our modeling, we sought to adjust for these sources of uncertainty and to facilitate interpretation. For glioma, when comparing those in the highest quartile of use (>558 lifetime hours) to those who were not regular users, the odds ratio was 2.0 (95% confidence interval: 1.2, 3.4). After adjustment for selection and recall biases, the odds ratio was 2.2 (95% limits: 1.3, 4.1). There was little evidence of an increase in the risk of meningioma, acoustic neuroma, or parotid gland tumors in relation to mobile phone use. Adjustments for selection and recall biases did not materially affect interpretation in our results from Canadian data. 10.1093/aje/kwx157
    Mobile phone radiation health risk controversy: the reliability and sufficiency of science behind the safety standards. Leszczynski Dariusz,Xu Zhengping Health research policy and systems There is ongoing discussion whether the mobile phone radiation causes any health effects. The International Commission on Non-Ionizing Radiation Protection, the International Committee on Electromagnetic Safety and the World Health Organization are assuring that there is no proven health risk and that the present safety limits protect all mobile phone users. However, based on the available scientific evidence, the situation is not as clear. The majority of the evidence comes from in vitro laboratory studies and is of very limited use for determining health risk. Animal toxicology studies are inadequate because it is not possible to "overdose" microwave radiation, as it is done with chemical agents, due to simultaneous induction of heating side-effects. There is a lack of human volunteer studies that would, in unbiased way, demonstrate whether human body responds at all to mobile phone radiation. Finally, the epidemiological evidence is insufficient due to, among others, selection and misclassification bias and the low sensitivity of this approach in detection of health risk within the population. This indicates that the presently available scientific evidence is insufficient to prove reliability of the current safety standards. Therefore, we recommend to use precaution when dealing with mobile phones and, whenever possible and feasible, to limit body exposure to this radiation. Continuation of the research on mobile phone radiation effects is needed in order to improve the basis and the reliability of the safety standards. 10.1186/1478-4505-8-2
    Mobile phone and cordless phone use and the risk for glioma - Analysis of pooled case-control studies in Sweden, 1997-2003 and 2007-2009. Hardell Lennart,Carlberg Michael Pathophysiology : the official journal of the International Society for Pathophysiology We made a pooled analysis of two case-control studies on malignant brain tumours with patients diagnosed during 1997-2003 and 2007-2009. They were aged 20-80 years and 18-75 years, respectively, at the time of diagnosis. Only cases with histopathological verification of the tumour were included. Population-based controls, matched on age and gender, were used. Exposures were assessed by questionnaire. The whole reference group was used in the unconditional regression analysis adjusted for gender, age, year of diagnosis, and socio-economic index. In total, 1498 (89%) cases and 3530 (87%) controls participated. Mobile phone use increased the risk of glioma, OR=1.3, 95% CI=1.1-1.6 overall, increasing to OR=3.0, 95% CI=1.7-5.2 in the >25 year latency group. Use of cordless phones increased the risk to OR=1.4, 95% CI=1.1-1.7, with highest risk in the >15-20 years latency group yielding OR=1.7, 95% CI=1.1-2.5. The OR increased statistically significant both per 100h of cumulative use, and per year of latency for mobile and cordless phone use. Highest ORs overall were found for ipsilateral mobile or cordless phone use, OR=1.8, 95% CI=1.4-2.2 and OR=1.7, 95% CI=1.3-2.1, respectively. The highest risk was found for glioma in the temporal lobe. First use of mobile or cordless phone before the age of 20 gave higher OR for glioma than in later age groups. 10.1016/j.pathophys.2014.10.001
    Mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the United States. Little M P,Rajaraman P,Curtis R E,Devesa S S,Inskip P D,Check D P,Linet M S BMJ (Clinical research ed.) OBJECTIVE:In view of mobile phone exposure being classified as a possible human carcinogen by the International Agency for Research on Cancer (IARC), we determined the compatibility of two recent reports of glioma risk (forming the basis of the IARC's classification) with observed incidence trends in the United States. DESIGN:Comparison of observed rates with projected rates of glioma incidence for 1997-2008. We estimated projected rates by combining relative risks reported in the 2010 Interphone study and a 2011 Swedish study by Hardell and colleagues with rates adjusted for age, registry, and sex; data for mobile phone use; and various latency periods. SETTING:US population based data for glioma incidence in 1992-2008, from 12 registries in the Surveillance, Epidemiology, and End Results (SEER) programme (Atlanta, Detroit, Los Angeles, San Francisco, San Jose-Monterey, Seattle, rural Georgia, Connecticut, Hawaii, Iowa, New Mexico, and Utah). PARTICIPANTS:Data for 24,813 non-Hispanic white people diagnosed with glioma at age 18 years or older. RESULTS:Age specific incidence rates of glioma remained generally constant in 1992-2008 (-0.02% change per year, 95% confidence interval -0.28% to 0.25%), a period coinciding with a substantial increase in mobile phone use from close to 0% to almost 100% of the US population. If phone use was associated with glioma risk, we expected glioma incidence rates to be higher than those observed, even with a latency period of 10 years and low relative risks (1.5). Based on relative risks of glioma by tumour latency and cumulative hours of phone use in the Swedish study, predicted rates should have been at least 40% higher than observed rates in 2008. However, predicted glioma rates based on the small proportion of highly exposed people in the Interphone study could be consistent with the observed data. Results remained valid if we used either non-regular users or low users of mobile phones as the baseline category, and if we constrained relative risks to be more than 1. CONCLUSIONS:Raised risks of glioma with mobile phone use, as reported by one (Swedish) study forming the basis of the IARC's re-evaluation of mobile phone exposure, are not consistent with observed incidence trends in US population data, although the US data could be consistent with the modest excess risks in the Interphone study. 10.1136/bmj.e1147
    Mobile phone use and risk of glioma: a case-control study in Korea for 2002-2007. Yoon Songyi,Choi Jae-Wook,Lee Eunil,An Hyonggin,Choi Hyong Do,Kim Nam Environmental health and toxicology OBJECTIVES:There has been a growing concern about the possible carcinogenic effects of the electromagnetic radiofrequency fields emitted from mobile phones. The purpose of this study was to investigate the association between mobile phone use and the development of gliomas in Korea. METHODS:Our study methods were based on the International Interphone study that aimed to evaluate possible adverse effects of mobile phone use. This study included 285 histologically-confirmed Korean patients 15 to 69 years of age, with gliomas diagnosed between 2002 and 2007 in 9 hospitals. The 285 individually matched controls were healthy individuals that had their medical check-up in the same hospitals. Unconditional logistic regression was used to calculate the adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for use of mobile phones. RESULTS:For the entire group, no significant relationship was investigated between gliomas and regular use of mobile phones, types of mobile phones, lifetime years of use, monthly service fee, and the other exposure indices. Analyses restricted to self-respondents showed similar results. For ipsilateral users, whose the body side for usual mobile phone use match the location of glioma, the aORs (95% CIs) for lifetime years of use and cumulative hours of use were 1.25 (0.55 to 2.88) and 1.77 (0.32 to 1.84), respectively. However, the contralateral users showed slightly lower risk than ipsilateral users. CONCLUSIONS:Our results do not support the hypothesis that the use of mobile phones increases the risk of glioma; however, we found a non-significant increase in risk among ipsilateral users. These findings suggest further evaluation for glioma risk among long-term mobile phone users. 10.5620/eht.e2015015
    Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill Viewpoints from 1965 on Association or Causation. Carlberg Michael,Hardell Lennart BioMed research international Bradford Hill's viewpoints from 1965 on association or causation were used on glioma risk and use of mobile or cordless phones. All nine viewpoints were evaluated based on epidemiology and laboratory studies. Strength: meta-analysis of case-control studies gave odds ratio (OR) = 1.90, 95% confidence interval (CI) = 1.31-2.76 with highest cumulative exposure. Consistency: the risk increased with latency, meta-analysis gave in the 10+ years' latency group OR = 1.62, 95% CI = 1.20-2.19. Specificity: increased risk for glioma was in the temporal lobe. Using meningioma cases as comparison group still increased the risk. Temporality: highest risk was in the 20+ years' latency group, OR = 2.01, 95% CI =1.41-2.88, for wireless phones. Biological gradient: cumulative use of wireless phones increased the risk. Plausibility: animal studies showed an increased incidence of glioma and malignant schwannoma in rats exposed to radiofrequency (RF) radiation. There is increased production of reactive oxygen species (ROS) from RF radiation. Coherence: there is a change in the natural history of glioma and increasing incidence. Experiment: antioxidants reduced ROS production from RF radiation. Analogy: there is an increased risk in subjects exposed to extremely low-frequency electromagnetic fields. RF radiation should be regarded as a human carcinogen causing glioma. 10.1155/2017/9218486
    Coffee and cancer risk, epidemiological evidence, and molecular mechanisms. Bøhn Siv Kjølsrud,Blomhoff Rune,Paur Ingvild Molecular nutrition & food research Although early studies suggested that coffee consumption might increase risk of some cancers, more comprehensive epidemiological and experimental data now generally indicate either neutral or beneficial effects. In this review, we summarize the current evidence for associations between breast, prostate, colorectal, and liver cancers and the consumption of coffee, and discuss the experimental evidence for potential chemopreventive mechanisms of coffee and coffee constituents. The epidemiological evidence consistently indicates that coffee protects against liver cancer, and also point toward protective effects for risk of colorectal cancers (with relative risks of 0.50 (95% CI: 0.42-0.59) and 0.83 (95% CI: 0.75-0.92), respectively, in the most recent meta-analyses). There seems to be no association between the overall risk of breast and prostate cancer and coffee intake. However, for subgroups such as postmenopausal breast cancers, advanced prostate cancers, and breast and prostate cancer survivors, an inverse association with coffee intake is indicated. Potential mechanisms for chemopreventive effects of coffee phytochemicals includes inhibition of oxidative stress and oxidative damage, regulation of DNA repair, phase II enzymatic activity, apoptosis, inflammation, as well as having antiproliferative, antiangiogenetic effects and antimetastatic effects. The experimental evidence for effects of coffee and coffee constituents on each of these processes is discussed. 10.1002/mnfr.201300526
    Coffee and tea intake and risk of brain tumors in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study. Michaud Dominique S,Gallo Valentina,Schlehofer Brigitte,Tjønneland Anne,Olsen Anja,Overvad Kim,Dahm Christina C,Teucher Birgit,Lukanova Annekatrin,Boeing Heiner,Schütze Madlen,Trichopoulou Antonia,Lagiou Pagona,Kyrozis Andreas,Sacerdote Carlotta,Krogh Vittorio,Masala Giovanna,Tumino Rosario,Mattiello Amalia,Bueno-de-Mesquita H Bas,Ros Martine M,Peeters Petra H M,van Gils Carla H,Skeie Guri,Engeset Dagrun,Parr Christine L,Ardanaz Eva,Chirlaque Maria-Dolores,Dorronsoro Miren,Sánchez Maria José,Argüelles Marcial,Jakszyn Paula,Nilsson Lena M,Melin Beatrice S,Manjer Jonas,Wirfält Elisabet,Khaw Kay-Tee,Wareham Nick,Allen Naomi E,Key Timothy J,Romieu Isabelle,Vineis Paolo,Riboli Elio The American journal of clinical nutrition BACKGROUND:In a recent US cohort study, total coffee and tea consumption was inversely associated with risk of glioma, and experimental studies showed that caffeine can slow the invasive growth of glioblastoma. OBJECTIVE:The objective was to examine the relation between coffee and tea intake and the risk of glioma and meningioma in a large European cohort study, the European Prospective Investigation into Cancer and Nutrition (EPIC). DESIGN:Data on coffee and tea intake were collected from men and women recruited into the EPIC cohort study. Over an average of 8.5 y of follow-up, 343 cases of glioma and 245 cases of meningioma were newly diagnosed in 9 countries. We used Cox proportional hazards models to examine the relation between coffee and tea and brain tumors. RESULTS:We observed no associations between coffee, tea, or combined coffee and tea consumption and risk of either type of brain tumor when using quantiles based on country-specific distributions of intake. However, a significant inverse association was observed for glioma risk among those consuming ≥100 mL coffee and tea per day compared with those consuming <100 mL/d (hazard ratio: 0.66; 95% CI: 0.44, 0.97; P = 0.03). The association was slightly stronger in men (hazard ratio: 0.59; 95% CI: 0.34, 1.01) than in women (hazard ratio: 0.74; 95% CI: 0.42, 1.31), although neither was statistically significant. CONCLUSIONS:In this large cohort study, we observed an inverse association between total coffee and tea consumption and risk of glioma that was consistent with the findings of a recent study. These findings, if further replicated in other studies, may provide new avenues of research on gliomas. 10.3945/ajcn.2010.29876
    Coffee, tea, and melanoma risk among postmenopausal women. Wu Haotian,Reeves Katherine W,Qian Jing,Sturgeon Susan R European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) Laboratory research suggests that components in coffee and tea may have anticarcinogenic effects. Some epidemiologic studies have reported that women who consume coffee and tea have a lower risk for melanoma. We assessed coffee, tea, and melanoma risk prospectively in the Women's Health Initiative - Observational Study cohort of 66,484 postmenopausal women, followed for an average of 7.7 years. Coffee and tea intakes were measured through self-administered questionnaires at baseline and at year 3 of follow-up. Self-reported incident melanomas were adjudicated using medical records. Cox proportional hazard models were used to estimate risk, adjusting for covariates, with person-time accumulation until melanoma diagnosis (n=398), death, loss to follow-up, or through 2005. Daily coffee [hazard ratio (HR)=0.87, 95% confidence interval (CI) 0.68-1.12] and tea (HR=1.03, 95% CI 0.81-1.31) intakes were not significantly associated with melanoma risk compared with nondaily intake of each beverage. No significant trends were observed between melanoma risk and increasing intakes of coffee (P for trend=0.38) or tea (P for trend=0.22). Women who reported daily coffee intake at both baseline and year 3 had a significantly decreased risk compared with women who reported nondaily intake at both time points (HR=0.68, 95% CI 0.48-0.97). Consistent daily tea intake was not associated with decreased melanoma risk. Overall, there is no strong evidence that increasing coffee or tea consumption can lead to a lower melanoma risk. We observed a decrease in melanoma risk among long-term coffee drinkers, but the lack of consistency in the results by dose and type cautioned against overinterpretation of the results. 10.1097/CEJ.0000000000000093
    Coffee, decaffeinated coffee, tea intake, and risk of renal cell cancer. Montella Maurizio,Tramacere Irene,Tavani Alessandra,Gallus Silvano,Crispo Anna,Talamini Renato,Dal Maso Luigino,Ramazzotti Valerio,Galeone Carlotta,Franceschi Silvia,La Vecchia Carlo Nutrition and cancer The relation between coffee, decaffeinated coffee, and tea intake and renal cell carcinoma (RCC) risk was analyzed in a case-control study conducted in Italy between 1992 and 2004. Cases were 767 subjects with incident histologically confirmed RCC and controls were 1,534 patients in hospital for acute non neoplastic conditions. Odds ratios (OR) and 95% confidence intervals (CI) for RCC were computed by multiple logistic regression models, conditioned on study center, sex, and age. Coffee intake (mostly espresso and mocha) was not associated with RCC risk, with an OR of 1.02 (95% CI 0.73-1.43) in drinkers of > or = 4 cups/day compared with drinkers of < 1 cup/day. The corresponding ORs were 1.34 (95% CI 0.87-2.07) in men and 0.67 (95% CI 0.38-1.18) in women, 1.91 (95% CI 0.85-4.31) in current smokers and 0.74 (95% CI 0.41-1.31) in never smokers, with no trend in risk with dose. No relation was observed with decaffeinated coffee (OR = 1.38, 95% CI 0.94-2.03 for drinkers compared with nondrinkers) and tea intake (OR = 0.78, 95% CI 0.59-1.05 for drinkers of > or = 1 cup/day compared with nondrinkers). No significant heterogeneity was found for coffee intake across strata of age, education, body mass index, and consumption of sugar. This study, based on a large dataset, provides further evidence that coffee, decaffeinated coffee, and tea consumption are not related to RCC risk. 10.1080/01635580802670754
    Coffee and cancer risk: a summary overview. Alicandro Gianfranco,Tavani Alessandra,La Vecchia Carlo European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) We reviewed available evidence on coffee drinking and the risk of all cancers and selected cancers updated to May 2016. Coffee consumption is not associated with overall cancer risk. A meta-analysis reported a pooled relative risk (RR) for an increment of 1 cup of coffee/day of 1.00 [95% confidence interval (CI): 0.99-1.01] for all cancers. Coffee drinking is associated with a reduced risk of liver cancer. A meta-analysis of cohort studies found an RR for an increment of consumption of 1 cup/day of 0.85 (95% CI: 0.81-0.90) for liver cancer and a favorable effect on liver enzymes and cirrhosis. Another meta-analysis showed an inverse relation for endometrial cancer risk, with an RR of 0.92 (95% CI: 0.88-0.96) for an increment of 1 cup/day. A possible decreased risk was found in some studies for oral/pharyngeal cancer and for advanced prostate cancer. Although data are mixed, overall, there seems to be some favorable effect of coffee drinking on colorectal cancer in case-control studies, in the absence of a consistent relation in cohort studies. For bladder cancer, the results are not consistent; however, any possible direct association is not dose and duration related, and might depend on a residual confounding effect of smoking. A few studies suggest an increased risk of childhood leukemia after maternal coffee drinking during pregnancy, but data are limited and inconsistent. Although the results of studies are mixed, the overall evidence suggests no association of coffee intake with cancers of the stomach, pancreas, lung, breast, ovary, and prostate overall. Data are limited, with RR close to unity for other neoplasms, including those of the esophagus, small intestine, gallbladder and biliary tract, skin, kidney, brain, thyroid, as well as for soft tissue sarcoma and lymphohematopoietic cancer. 10.1097/CEJ.0000000000000341
    Coffee consumption and risk of renal cell carcinoma. Antwi Samuel O,Eckel-Passow Jeanette E,Diehl Nancy D,Serie Daniel J,Custer Kaitlynn M,Arnold Michelle L,Wu Kevin J,Cheville John C,Thiel David D,Leibovich Bradley C,Parker Alexander S Cancer causes & control : CCC BACKGROUND:Studies have suggested an inverse association between coffee consumption and risk of renal cell carcinoma (RCC); however, data regarding decaffeinated coffee are limited. METHODS:We conducted a case-control study of 669 incident RCC cases and 1,001 frequency-matched controls. Participants completed identical risk factor questionnaires that solicited information about usual coffee consumption habits. The study participants were categorized as non-coffee, caffeinated coffee, decaffeinated coffee, or both caffeinated and decaffeinated coffee drinkers. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression, adjusting for multiple risk factors for RCC. RESULTS:Compared with no coffee consumption, we found an inverse association between caffeinated coffee consumption and RCC risk (OR 0.74; 95% CI 0.57-0.99), whereas we observed a trend toward increased risk of RCC for consumption of decaffeinated coffee (OR 1.47; 95% CI 0.98-2.19). Decaffeinated coffee consumption was associated also with increased risk of the clear cell RCC (ccRCC) subtype, particularly the aggressive form of ccRCC (OR 1.80; 95% CI 1.01-3.22). CONCLUSIONS:Consumption of caffeinated coffee is associated with reduced risk of RCC, while decaffeinated coffee consumption is associated with an increase in risk of aggressive ccRCC. Further inquiry is warranted in large prospective studies and should include assessment of dose-response associations. 10.1007/s10552-017-0913-z
    Coffee and green tea consumption in relation to brain tumor risk in a Japanese population. Ogawa Takahiro,Sawada Norie,Iwasaki Motoki,Budhathoki Sanjeev,Hidaka Akihisa,Yamaji Taiki,Shimazu Taichi,Sasazuki Shizuka,Narita Yoshitaka,Tsugane Shoichiro, International journal of cancer Few prospective studies have investigated the etiology of brain tumor, especially among Asian populations. Both coffee and green tea are popular beverages, but their relation with brain tumor risk, particularly with glioma, has been inconsistent in epidemiological studies. In this study, we evaluated the association between coffee and greed tea intake and brain tumor risk in a Japanese population. We evaluated a cohort of 106,324 subjects (50,438 men and 55,886 women) in the Japan Public Health Center-Based Prospective Study (JPHC Study). Subjects were followed from 1990 for Cohort I and 1993 for Cohort II until December 31, 2012. One hundred and fifty-seven (70 men and 87 women) newly diagnosed cases of brain tumor were identified during the study period. Hazard ratio (HR) and 95% confidence intervals (95%CIs) for the association between coffee or green tea consumption and brain tumor risk were assessed using a Cox proportional hazards regression model. We found a significant inverse association between coffee consumption and brain tumor risk in both total subjects (≥3 cups/day; HR = 0.47, 95%CI = 0.22-0.98) and in women (≥3 cups/day; HR = 0.24, 95%CI = 0.06-0.99), although the number of cases in the highest category was small. Furthermore, glioma risk tended to decrease with higher coffee consumption (≥3 cups/day; HR = 0.54, 95%CI = 0.16-1.80). No association was seen between green tea and brain tumor risk. In conclusion, our study suggested that coffee consumption might reduce the risk of brain tumor, including that of glioma, in the Japanese population. 10.1002/ijc.30405
    Coffee, tea, soda, and caffeine intake in relation to risk of adult glioma in the NIH-AARP Diet and Health Study. Dubrow Robert,Darefsky Amy S,Freedman Neal D,Hollenbeck Albert R,Sinha Rashmi Cancer causes & control : CCC PURPOSE:We utilized the large, prospective NIH-AARP Diet and Health Study to further explore the hypothesis, suggested by two recent prospective cohort studies, that increased intake of coffee, tea, soda, and/or caffeine is associated with reduced adult glioma risk. METHODS:At baseline in 1995-1996, dietary intake, including coffee, tea, and soda, was assessed with a food frequency questionnaire. We used Cox proportional hazards models to calculate adjusted hazard ratios (HR) and 95 % confidence intervals (CI) for glioma risk in relation to beverage intake. RESULTS:During follow-up of 545,771 participants through 2006, 904 participants were diagnosed with glioma. We found no trends of decreasing glioma risk with increasing intake of specific beverages or total caffeine. HR patterns for consumption of the caffeinated versus decaffeinated form of each beverage were inconsistent with a specific caffeine effect. HR patterns of reduced glioma risk for most categories of beverage intake greater than "none" prompted a post hoc analysis that revealed borderline-significant inverse associations for any versus no intake of tea (HR = 0.84; 95 % CI, 0.69-1.03), total coffee plus tea (HR = 0.70; 95 % CI, 0.48-1.03), and soda (HR = 0.82; 95 % CI, 0.67-1.01). CONCLUSIONS:The borderline-significant inverse associations could be explained by a threshold effect in which any beverage intake above a low level confers a beneficial effect, most likely due to beverage constituents other than caffeine. They could also be explained by non-drinkers of these beverages sharing unknown extraneous characteristics associated with increased glioma risk, or by chance. 10.1007/s10552-012-9945-6
    [Alcohol Use and Cancer Risk]. Scherübl Hans Deutsche medizinische Wochenschrift (1946) Alcohol use is one of the most important and potentially modifiable risk factors for cancer in Germany. The more and the longer a person drinks, the higher the risk of cancer. Even modest use of alcohol may increase cancer risk. Statistically, every German drinks more than 100 gram of alcohol per week; this amount is currently considered to be the limit of low-risk use. Alcohol is causally associated with oropharyngeal and larynx cancer, esophageal squamous cell cancer, hepatocellular carcinoma, breast cancer, and colorectal cancer. People with long-term risky alcohol use should be encouraged to join programs of cancer screening. Alcohol cessation appears to be effective in reducing the alcohol-induced, increased cancer risk. 10.1055/a-0928-0586
    Tobacco smoking and alcohol consumption as risk factors for glioma: a case-control study in Melbourne, Australia. Hurley S F,McNeil J J,Donnan G A,Forbes A,Salzberg M,Giles G G Journal of epidemiology and community health OBJECTIVE:To investigate possible associations between tobacco smoking and alcohol consumption and the risk of adult glioma. DESIGN:This was a population based, case-control study. Relative risks (RR) were estimated using logistic regression analysis. SETTING:Melbourne, Australia. PARTICIPANTS:These comprised 416 case subjects (166 women, 250 men), 66% of those eligible; and 422 control subjects (170 women, 252 men), 43.5% of those potentially eligible. RESULTS:There was no increase in risk of glioma with having ever smoked tobacco (RR 1.29, 95% CI 0.95, 1.75) for all subjects, adjusted for age, a reference date, and gender. There was a slight increase in risk for men (RR 1.64, 95% CI 1.1, 2.45), but not for women (RR 0.99, 95% CI 0.62, 1.62). For men, there was no increase in risk with increasing pack-years of cigarette smoking, but the risk was significantly increased in subjects who had smoked for less than 10 years. There was no increase in risk associated with having ever drunk alcohol for all subjects (RR 0.96, 95% CI 0.67, 1.37), women (RR 0.69, 95% CI 0.4, 1.15) or men (RR 1.40, 95% CI 0.81, 2.43). CONCLUSIONS:This study does not support an association between either tobacco smoking or alcohol consumption and glioma. The pattern of risk associated with tobacco smoking in men appears inconsistent with a causal role, and may be due to chance, response bias, or uncontrolled confounding. 10.1136/jech.50.4.442
    Tea and cancer prevention: epidemiological studies. Yuan Jian-Min,Sun Canlan,Butler Lesley M Pharmacological research Experimental studies have consistently shown the inhibitory activities of tea extracts on tumorigenesis in multiple model systems. Epidemiological studies, however, have produced inconclusive results in humans. A comprehensive review was conducted to assess the current knowledge on tea consumption and risk of cancers in humans. In general, consumption of black tea was not associated with lower risk of cancer. High intake of green tea was consistently associated with reduced risk of upper gastrointestinal tract cancers after sufficient control for confounders. Limited data support a protective effect of green tea on lung and hepatocellular carcinogenesis. Although observational studies do not support a beneficial role of tea intake on prostate cancer risk, phase II clinical trials have demonstrated an inhibitory effect of green tea extract against the progression of prostate pre-malignant lesions. Green tea may exert beneficial effects against mammary carcinogenesis in premenopausal women and recurrence of breast cancer. There is no sufficient evidence that supports a protective role of tea intake on the development of cancers of the colorectum, pancreas, urinary tract, glioma, lymphoma, and leukemia. Future prospective observational studies with biomarkers of exposure and phase III clinical trials are required to provide definitive evidence for the hypothesized beneficial effect of tea consumption on cancer formation in humans. 10.1016/j.phrs.2011.03.002
    Tea, coffee and risk of glioma. Kawada Tomoyuki EXCLI journal 10.17179/excli2020-2865
    Effects of the Green Tea Polyphenol Epigallocatechin-3-Gallate on Glioma: A Critical Evaluation of the Literature. Le Chung T,Leenders William P J,Molenaar Remco J,van Noorden Cornelis J F Nutrition and cancer The review discusses the effects of Epigallocatechin-3-gallate Gallate (EGCG) on glioma as a basis for future research on clinical application of EGCG. Epidemiological studies on the effects of green tea or EGCG on the risk of glioma is inconclusive due to the limited number of studies, the inclusion of all tea types in these studies, and the focus on caffeine rather than EGCG. In vivo experiments using EGCG monotherapy are inconclusive. Nevertheless, EGCG induces cell death, prevents cellular proliferation, and limits invasion in multiple glioma cell lines. Furthermore, EGCG enhances the efficacy of anti-glioma therapies, including irradiation, temozolomide, carmustine, cisplatin, tamoxifen, and TNF-related apoptosis-inducing ligand, but reduces the effect of bortezomib. Pro-drugs, co-treatment, and encapsulation are being investigated to enhance clinical applicability of EGCG. Mechanisms of actions of EGCG have been partly elucidated. EGCG has both anti-oxidant and oxidant properties. EGCG inhibits pro-survival proteins, such as telomerase, survivin, GRP78, PEA15, and P-gp. EGCG inhibits signaling of PDGFR, IGF-1R, and 67LR. EGCG reduces invasiveness of cancer cells by inhibiting the activities of various metalloproteinases, cytokines, and chemokines. Last, EGCG inhibits some NADPH-producing enzymes, thus disturbing redox status and metabolism of glioma cells. In conclusion, EGCG may be a suitable adjuvant to potentiate anti-glioma therapies. 10.1080/01635581.2018.1446090
    A meta-analysis of coffee and tea consumption and the risk of glioma in adults. Malerba Stefano,Galeone Carlotta,Pelucchi Claudio,Turati Federica,Hashibe Mia,La Vecchia Carlo,Tavani Alessandra Cancer causes & control : CCC BACKGROUND:Coffee contains many compounds, including antioxidants, which could prevent cancerogenesis, and coffee has been related with lower incidence of cancer at several sites. Tea is also rich in antioxidants, mainly polyphenols. To provide a quantitative overall estimate on the relation between coffee and tea consumption and glioma, we combined all published data, using a meta-analytic approach. METHODS:In September 2012, a bibliography search was carried out in both PubMed and Embase to identify observational studies providing quantitative estimates on the issue. Pooled estimates of the relative risks (RR) and the corresponding 95 % confidence intervals (CI) were calculated using random-effects models. RESULTS:Six studies (four cohort and two case-control studies) were available for meta-analysis, for a total of about 2100 cases. The summary RRs and 95 % CIs of glioma for drinkers versus non/occasional drinkers were 0.96 (95 % CI: 0.81-1.13) for coffee and 0.86 (95 % CI: 0.78-0.94) for tea, with no heterogeneity between studies. When we compared the highest versus the lowest categories of consumption, the RRs were 1.01 (95 % CI: 0.83-1.22) for coffee, 0.88 (95 % CI: 0.69-1.12) for tea, and 0.75 (95 % CI: 0.54-1.05) for coffee plus tea. CONCLUSIONS:This meta-analysis, although based on few studies, suggests a lack of association between coffee intake and glioma risk, and a tendency, if any, to a lower risk for tea and coffee plus tea drinkers. 10.1007/s10552-012-0126-4
    Tea and coffee consumption in relation to glioma: a case-control study. Malmir Hanieh,Shayanfar Mehdi,Mohammad-Shirazi Minoo,Tabibi Hadi,Sharifi Giuve,Esmaillzadeh Ahmad European journal of nutrition PURPOSE:Data on the link between tea and coffee consumption and risk of glioma are controversial. We aimed to examine the association between tea and coffee consumption and glioma in Iranian adults. METHODS:In this hospital-based case-control study, we enrolled 128 pathologically confirmed new cases of glioma and 256 age- and sex-matched controls. Dietary intakes of study participants including tea and coffee consumption was assessed using the validated Block-format 123-item semi-quantitative FFQ. Participants were categorized based on tertiles of tea and coffee consumption. Data on potential confounders were also collected through the use of pre-tested questionnaire. RESULTS:Individuals with the greatest tea consumption were less likely to have glioma compared with those with the lowest consumption (0.36; 0.20-0.68). This inverse association was not changed after controlling for energy intake. The association remained statistically significant even after taking other potential confounders, including dietary intakes of red and processed meats, legumes and nuts, fruits, salt and mutual effects of tea and coffee consumption, into account (0.33; 0.13-0.86). Additional adjustments for BMI did not alter the association. After controlling for potential confounders, including dietary intakes and BMI, coffee consumption was inversely associated with odds of glioma; such that individuals in the top category of coffee consumption were 91% less likely to have glioma compared with those in the bottom category (0.09; 0.03-0.24). Considering coffee and tea intake combined, those in the highest tertile were 65% less likely to have glioma compared with those in the lowest tertile (0.35; 0.15-0.83). CONCLUSION:We found an inverse association between tea and coffee consumption and odds of glioma, even after controlling for a wide range of confounders. 10.1007/s00394-017-1575-z
    Risk for use of antidepressants, anxiolytics, and hypnotics in partners of glioma patients-A nationwide study covering 19 years of prescriptions. Jansson Maria R N,von Heymann-Horan Annika,Rasmussen Birthe K,Albieri Vanna,Frederiksen Kirsten,Suppli Nis,Dalton Susanne O,Johansen Christoffer,Bidstrup Pernille E Psycho-oncology OBJECTIVE:Suffering from malignant brain tumor is a stressful condition, for patients and their partners. In a retrospective cohort study using nationwide registries, we examined partners' risk for first use of antidepressants, anxiolytics, or hypnotics. METHODS:We followed all 4373 partners of adults with glioma, diagnosed in 1998 to 2013 in Denmark and a cohort of 43 808 partners of glioma-free persons matched 1:10. In Cox proportional hazard models, we estimated hazard ratios (HRs) for a first prescription of psychotropic medications (antidepressants, anxiolytics, or hypnotics) according to the partner's glioma status. Among partners of glioma patients, we further estimated HRs for a first prescription of psychotropic medication according to disease characteristics, sociodemographic factors, and bereavement. RESULTS:Two years after diagnosis, 29% of female and 21% of male partners of glioma patients had had a first prescription of psychotropic medication compared with 10% in female and 8% in male partners of glioma-free persons. Partners of glioma patients had a significantly increased, 4-fold higher risk for a first prescription of psychotropic medications in the first year after diagnosis than partners of glioma-free persons (HR 4.10, 95% CI, 3.80:4.43). Among partners of glioma patients, the risk was significantly reduced in bereaved compared with non-bereaved partners. CONCLUSIONS:We have documented, for the first time, that the psychological impact of a diagnosis of glioma is such a severe stress exposure that it increases the risk for having medication prescribed to treat symptoms of anxiety, sleep problems, and depression. 10.1002/pon.4744
    Cell phone use and the risk of glioma: are case-control study findings consistent with Canadian time trends in cancer incidence? Villeneuve Paul J,Momoli Franco,Parent Marie-Élise,Siemiatycki Jack,Turner Michelle C,Krewski Daniel Environmental research BACKGROUND:There remains controversy as to whether cell phones cause cancer. We evaluated whether temporal changes in cell phone use and the incidence of glioma in Canada were consistent with the hypothesis of an increased risk. DESIGN:We used data from the Canadian Cancer Registry to calculate annual incidence rates for glioma between 1992 and 2015. The annual number of new cell phone subscribers was determined using national industry statistics. The number of newly diagnosed gliomas was compared to the predicted number by applying risks from epidemiological studies to age-specific population estimates. Specifically, we calculated the "predicted" number of incident gliomas by determining the annual prevalence of cell phone users and years of use. These estimates were multiplied by the corresponding risk estimates to determine the predicted number of gliomas. RESULTS:The number of cellular subscriptions in Canada increased from nil in the early-1980s to approximately 29.5 million in 2015. In contrast, age-standardized glioma incidence rates remained stable between 1992 and 2015. When applying risk estimates from i) a recent pooled analysis of Swedish case-control studies, ii) the 13 country INTERPHONE study, and iii) more recent results from data collected from the Canadian component of the INTERPHONE these risks overestimated the observed number of glioma cases diagnosed in Canada in 2015 by 50%, 86%, and 63%, respectively. INTERPRETATION:Predictions of glioma incidence counts using estimates of the relative risk of glioma due to cell phone use from case-control studies over-estimated the incidence rates of glioma in Canada. The absence of an elevation in incidence rates of glioma in conjunction with marked increases in cell phone use suggests that there may not be a causal link between cellphones and glioma. 10.1016/j.envres.2021.111283
    Interaction of allergy history and antibodies to specific varicella-zoster virus proteins on glioma risk. Lee Seung-Tae,Bracci Paige,Zhou Mi,Rice Terri,Wiencke John,Wrensch Margaret,Wiemels Joseph International journal of cancer Glioma is the most common cancer of the central nervous system but with few confirmed risk factors. It has been inversely associated with chicken pox, shingles and seroreactivity to varicella virus (VZV), as well as to allergies and allergy-associated IgE. The role of antibody reactivity against individual VZV antigens has not been assessed. Ten VZV-related proteins, selected for high immunogenicity or known function, were synthesized and used as targets for antibody measurements in the sera of 143 glioma cases and 131 healthy controls selected from the San Francisco Bay Area Adult Glioma Study. Glioma cases exhibited significantly reduced seroreactivity compared to controls for six antigens, including proteins IE63 [odds ratio (OR) = 0.26, 95% confidence interval (CI): 0.12-0.58, comparing lowest quartile to highest) and the VZV-unique protein ORF2p (OR = 0.44, 95% CI: 0.21-0.96, lowest quartile to highest). When stratifying the study population into those with low and high self-reported allergy history, VZV protein seroreactivity was only associated inversely with glioma among individuals self-reporting more than two allergies. The data provide insight into both allergy and VZV effects on glioma: strong anti-VZV reactions in highly allergic individuals are associated with reduced occurrence of glioma. This result suggests a role for specificity in the anti-VZV immunity in brain tumor suppression for both individual VZV antigens and in the fine-tuning of the immune response by allergy. Anti-VZV reactions may also be a biomarker of effective CNS immunosurveillance owing to the tropism of the virus. 10.1002/ijc.28535
    Association between Dietary Vitamin A Intake and the Risk of Glioma: Evidence from a Meta-analysis. Lv Wen,Zhong Xian,Xu Lingmin,Han Weidong Nutrients The results from epidemiological studies between dietary vitamin A intake and glioma risk is not consistent. Thus, a meta-analysis was conducted to confirm the exact relationship between them. PubMed and Web of Knowledge were used to search the relevant articles up to May 2015. Pooled relative risk (RR) with 95% confidence interval (CI)was calculated using random-effect model. Egger's test was used to assess the small-study effect. At the end, seven articles with eight case-control studies involving 1841 glioma cases and 4123 participants were included. Our study indicated that highest category of dietary vitamin A intake was significantly associated with reduced risk of glioma (RR = 0.80, 95% CI = 0.62-0.98, p = 0.014, I² = 54.9%). Egger's test did not find any publication bias. In conclusion, our study indicated that higher category of dietary vitamin A intake could reduce the glioma risk. However, we could not do a dose-response analysis for vitamin A intake with glioma risk due to the limited data in each reported individual article. Due to this limitation, further studies with detailed dose, cases and person-years for each category is wanted to assess this dose-response association. 10.3390/nu7115438
    Association between processed meat and red meat consumption and risk for glioma: a meta-analysis from 14 articles. Wei Youdong,Zou Dezhi,Cao Du,Xie Peng Nutrition (Burbank, Los Angeles County, Calif.) OBJECTIVE:Epidemiologic studies evaluating the association between processed meat and red meat consumption and glioma risk have produced inconsistent results. Thus, the aim of this study was to conduct a meta-analysis to test the hypothesis that high levels of processed meat consumption could increase the risk for glioma. METHODS:Pertinent studies were identified by a search of PubMed and Web of Knowledge up to February 2014. Random-effects model was used to combine the results. Publication bias was estimated using Egger's regression asymmetry test. RESULTS:Fourteen studies involving 3641 cases about processed meat consumption and 3 studies involving 1156 cases about red meat consumption with risk for glioma were included in this meta-analysis. The combined relative risk (RR) of glioma associated with processed meat consumption was 1.25 (95% confidence interval [CI], 1.08-1.45) overall, and 1.28 (95% CI, 1.09-1.50) in the United States. For subgroup of study design, significant association was also found in case-control studies (RR, 1.33; 95% CI, 1.09-1.62), but not in the cohort studies. The association was not significant between red meat consumption and glioma risk (summary RR, 0.89; 95% CI, 0.71-1.12). No publication biases were found. CONCLUSIONS:Our analysis indicated that high levels of processed meat consumption might increase the risk for glioma, and findings are consistent with the hypothesis. No association was found between red meat consumption and glioma risk. 10.1016/j.nut.2014.04.022
    Prospective study of intake of fruit, vegetables, and carotenoids and the risk of adult glioma. Holick Crystal N,Giovannucci Edward L,Rosner Bernard,Stampfer Meir J,Michaud Dominique S The American journal of clinical nutrition BACKGROUND:Nutrients in dietary fruit and vegetables have been hypothesized to lower the risk of glioma by reducing the endogenous formation of N-nitroso compounds. Studies examining fruit and vegetable consumption and brain tumors have relied on case-control study designs, with one exception, and results have been inconsistent. OBJECTIVE:We prospectively examined the relation between consumption of fruit and vegetables (and specifically carotenoids) and the risk of glioma among men and women in 3 large US cohort studies: the Health Professionals Follow-Up Study (HPFS), the Nurses' Health Study I (NHS I), and NHS II. DESIGN:Dietary intake was assessed by food-frequency questionnaires obtained at baseline and updated every 4 y through 2002 (HPFS and NHS I) or 2003 (NHS II). We identified 296 incident adult gliomas during 3 669 589 person-years of follow-up. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% CIs between intake of fruit, vegetables, and carotenoids and glioma risk, with adjustment for age and total caloric intake. RESULTS:Updated average consumption of total fruit and vegetables was not significantly associated with glioma risk in the men and women (pooled multivariate RR in a comparison of the highest with the lowest quintile: 1.12; 95% CI: 0.74, 1.69). Other fruit and vegetable subgroups, individual fruit and vegetables, and 5 major carotenoids were not significantly associated with risk of glioma. CONCLUSION:Our findings suggest that fruit, vegetable, and carotenoid consumption is not likely associated strongly with the risk of adult glioma. 10.1093/ajcn/85.3.877
    Occupation and the risk of adult glioma in the United States. De Roos A J,Stewart P A,Linet M S,Heineman E F,Dosemeci M,Wilcosky T,Shapiro W R,Selker R G,Fine H A,Black P M,Inskip P D Cancer causes & control : CCC OBJECTIVE:Previous studies have observed increased glioma incidence associated with employment in the petroleum and electrical industries, and in farming. Several other occupations have also been associated with increased risk, but with inconsistent results. We evaluated associations between occupational title and glioma incidence in adults. METHODS:Cases were 489 patients with glioma diagnosed from 1994 to 1998 at three United States hospitals. Controls were 799 patients admitted to the same hospitals for non-malignant conditions. An experienced industrial hygienist grouped occupations that were expected to have similar tasks and exposures. The risk of adult glioma was evaluated for those subjects who ever worked in an occupational group for at least six months, those who worked longer than five years in the occupation, and those with more than ten years latency since starting work in the occupation. RESULTS:Several occupational groups were associated with increased glioma incidence for having ever worked in the occupation, including butchers and meat cutters (odds ratio [OR] = 2.4; 95% confidence limits [CL]: 1.0, 6.0), computer programmers and analysts (OR = 2.0; 95% CL: 1.0, 3.8), electricians (OR = 1.8; 95% CL: 0.8, 4.1), general farmers and farmworkers (OR = 2.5; 95% CL: 1.4, 4.7), inspectors, checkers, examiners, graders, and testers (OR = 1.5; 95% CL: 0.8, 2.7), investigators, examiners, adjustors, and appraisers (OR = 1.7; 95% CL: 0.8, 3.7), physicians and physician assistants (OR = 2.4; 95% CL: 0.8, 7.2), and store managers (OR = 1.6; 95% CL: 0.8, 3.1), whereas occupation as a childcare worker was associated with decreased glioma incidence (OR = 0.4; 95% CL: 0.2, 0.9). These associations generally persisted when the subjects worked longer than five years in the occupation, and for those with more than ten years latency since starting to work in the occupation. CONCLUSIONS:This is our first analysis of occupation and will guide future exposure-specific assessments. 10.1023/a:1023053916689
    Drinking water and dietary sources of nitrate and nitrite and risk of glioma. Ward Mary H,Heineman Ellen F,McComb Rodney D,Weisenburger Dennis D Journal of occupational and environmental medicine OBJECTIVE:Dietary nitrite has been associated with increased glioma risk; however, drinking water nitrate has not been extensively evaluated. METHODS:We conducted a population-based case-control study of adult glioma in Nebraska. Water utility nitrate measurements were linked to residential water source histories. We computed average nitrate exposure over a 20-year period. A food frequency questionnaire was used to assess dietary nitrate and nitrite. RESULTS:Increasing quartiles of the average nitrate level in drinking water were not significantly associated with risk (adjusted odd ratios: 1.4, 1.2, 1.3). Risk was similar among those with both higher and lower intakes of vitamin C, an inhibitor of N-nitroso compound formation. Dietary nitrite intake was not associated with risk. CONCLUSIONS:Our study does not support a role for drinking water and dietary sources of nitrate and nitrite in risk of adult glioma.
    Birth month and risk of glioma in adults: a registry-based study in Bavaria. Staykov Dimitre,Radespiel-Tröger Martin,Meyer Martin,Petsch Sabrina,Schwab Stefan,Handschu René Chronobiology international The aim of the present study was to evaluate the possible seasonality of birth in adult patients suffering from glioma. For this purpose, data from the database of the population-based cancer registry of Bavaria (Germany) were retrieved. For the period 2002-2005, we identified a total of 2174 patients born between 1931 and 1986 diagnosed with malignant glioma. Statistical analyses failed to document a significant annual periodicity of glioma risk in either men or women with respect to birth month in the observed cohort. Thus, we found no association between month of birth and the risk of glioma. In contrast, an analysis of the official birth rate data of Bavaria revealed marked annual variation in birth rates up until 1965, which decreased markedly in prominence in the years thereafter. Our findings confirm the results of a recent similar study conducted in The Netherlands. Therefore, we support the hypothesis of possible etiological factors of glioma acting in adulthood rather than in the perinatal period. 10.1080/07420520902761778
    Diet and risk of glioma: combined analysis of 3 large prospective studies in the UK and USA. Kuan Ai Seon,Green Jane,Kitahara Cari M,Berrington De González Amy,Key Tim,K Reeves Gillian,Floud Sarah,Balkwill Angela,Bradbury Kathryn,Liao Linda M,Freedman Neal D,Beral Valerie,Sweetland Siân, Neuro-oncology BACKGROUND:Available evidence on diet and glioma risk comes mainly from studies with retrospective collection of dietary data. To minimize possible differential dietary recall between those with and without glioma, we present findings from 3 large prospective studies. METHODS:Participants included 692 176 from the UK Million Women Study, 470 780 from the US National Institutes of Health-AARP study, and 99 148 from the US Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cox regression yielded study-specific adjusted relative risks for glioma in relation to 15 food groups, 14 nutrients, and 3 dietary patterns, which were combined, weighted by inverse variances of the relative risks. Separate analyses by <5 and ≥5 years follow-up assessed potential biases related to changes of diet before glioma diagnosis. RESULTS:The 1 262 104 participants (mean age, 60.6 y [SD 5.5] at baseline) were followed for 15.4 million person-years (mean 12.2 y/participant), during which 2313 incident gliomas occurred, at mean age 68.2 (SD 6.4). Overall, there was weak evidence for increased glioma risks associated with increasing intakes of total fruit, citrus fruit, and fiber and healthy dietary patterns, but these associations were generally null after excluding the first 5 years of follow-up. There was little evidence for heterogeneity of results by study or by sex. CONCLUSIONS:The largest prospective evidence to date suggests little, if any, association between major food groups, nutrients, or common healthy dietary patterns and glioma incidence. With the statistical power of this study and the comprehensive nature of the investigation here, it seems unlikely we have overlooked major effects of diet on risk of glioma that would be of public health concern. 10.1093/neuonc/noz013
    Dietary fresh fish and processed fish intake and the risk of glioma: A meta-analysis of observational studies. Zhang Zihe,Xin Jiangze Cellular and molecular biology (Noisy-le-Grand, France) The current study was to evaluate the predicted role of dietary fresh fish and processed fish intake for risk of glioma. Databases of Web of Science, PubMed, and Wan Fang Med Online were retrieved up to Jan 31th, 2018. Eligible studies were identified based on defined inclusion criteria. Summarized results of relative risk (RR) with corresponding 95% confidence intervals (CI) were calculated using a random effects model. Sensitivity analysis and publication bias were also performed. The final analysis in this report included a total of 9 articles. The summarized RR and 95%CI from 8 studies for dietary fresh fish intake and glioma risk was 0.823 (95%CI= 0.698-0.970), with no evidence of significant between-study heterogeneity (I2=43.6%, P=0.088). Moreover, positive associations were also found both in Caucasian populations and Asia populations. Seven studies were used to assess the relationship between dietary processed fish intake and the risk of glioma. Significantly increased risk of glioma was found for the highest category of dietary processed fish intake [summarized RR= 1.554, 95%CI= 1.169-2.066, I2= 72.1%, P= 0.001], especially among Caucasian populations. No publication bias was found. In summary, findings from this meta-analysis concluded that dietary fresh fish intake could reduce the risk of glioma. However, very high processed fish intake had a significant association with increased glioma risk.
    Long-term anti-inflammatory and antihistamine medication use and adult glioma risk. Scheurer Michael E,El-Zein Randa,Thompson Patricia A,Aldape Kenneth D,Levin Victor A,Gilbert Mark R,Weinberg Jeffrey S,Bondy Melissa L Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology A personal history of asthma or allergy has been associated with a reduced risk for adult malignant gliomas. Recent reports on the use of nonsteroidal anti-inflammatory drugs (NSAID) and the presence of risk alleles in asthma susceptibility genes showed similar inverse associations. To further explore the relationship between immune mediators and gliomas, we examined the use of NSAID and antihistamines, history of asthma or allergy, and infection in 325 glioma cases and 600 frequency-matched controls from the metropolitan area of Houston, TX (2001-2006). The regular use of NSAID was associated with a 33% reduction in the risk for glioma, suggestive of possible antitumor activity. Surprisingly, regular long-term antihistamine use among those reporting a history of asthma or allergies was significantly associated with a 3.5-fold increase in the risk for glioma. Similar to previous reports, cases in our study were less likely to have reported asthma, allergy, or a history of a number of viral infections (chickenpox or shingles, oral herpes, and mononucleosis) than controls. We therefore speculate that the observed positive association with antihistamine use may reflect an alteration of protective immune factors in susceptible individuals. Our results lend additional support for an important but unknown link between malignant brain tumors and immune mediators. 10.1158/1055-9965.EPI-07-2621
    Mobile phone use and risk of glioma in adults: case-control study. Hepworth Sarah J,Schoemaker Minouk J,Muir Kenneth R,Swerdlow Anthony J,van Tongeren Martie J A,McKinney Patricia A BMJ (Clinical research ed.) OBJECTIVE:To investigate the risk of glioma in adults in relation to mobile phone use. DESIGN:Population based case-control study with collection of personal interview data. SETTING:Five areas of the United Kingdom. PARTICIPANTS:966 people aged 18 to 69 years diagnosed with a glioma from 1 December 2000 to 29 February 2004 and 1716 controls randomly selected from general practitioner lists. MAIN OUTCOME MEASURES:Odds ratios for risk of glioma in relation to mobile phone use. RESULTS:The overall odds ratio for regular phone use was 0.94 (95% confidence interval 0.78 to 1.13). There was no relation for risk of glioma and time since first use, lifetime years of use, and cumulative number of calls and hours of use. A significant excess risk for reported phone use ipsilateral to the tumour (1.24, 1.02 to 1.52) was paralleled by a significant reduction in risk (0.75, 0.61 to 0.93) for contralateral use. CONCLUSIONS:Use of a mobile phone, either in the short or medium term, is not associated with an increased risk of glioma. This is consistent with most but not all published studies. The complementary positive and negative risks associated with ipsilateral and contralateral use of the phone in relation to the side of the tumour might be due to recall bias. 10.1136/bmj.38720.687975.55
    A case-control study of the association between the gene and glioma risk in a Chinese Han population. Yan Mengdan,Li Jingjie,He Na,Shi Xugang,Du Shuli,Li Bin,Jin Tianbo Oncotarget The Epidermal Growth Factor Receptor gene has been reported to be involved in the progression of gliomas which is one of the deadliest primary brain tumors in humans. To determine potential association between and glioma risk, we performed a case-control study with 394 glioma patients and 298 cancer-free controls in which captured a total of 8 tag single nucleotide polymorphisms of gene from Xi'an, China. SPSS 19.0 statistical packages, χ test, genetic model analysis and SHEsis software platform were analyzed s the variants in gene associations with glioma risk. For five different inheritance models analyzed, the following genotypes were associated with increased glioma risk. In the codominant model, genotype CC (rs730437, OR = 1.93, = 0.024; rs1468727, OR = 2.02, = 0.007); In the dominant model, genotype CA and CC (rs730437, OR = 1.45, = 0.026), genotype GA and AA (rs845552, OR = 1.40, = 0.044); In the recessive model, genotype CC (rs730437, OR = 1.64, = 0.026; rs1468727, OR = 1.87, = 0.002); In the additive model, genotype CC (rs730437, OR = 1.32, = 0.006; rs1468727, OR = 1.39, = 0.005), genotype GG (rs11506105, OR = 1.32, = 0.02) and genotype AA (rs845552, OR = 1.27, = 0.04). Our study indicated that 8 mutants located in gene were risk-conferring factors, larger and different populations with polymorphisms are required to verify these associations. 10.18632/oncotarget.16946
    Mobile phone use and risk of glioma in 5 North European countries. Lahkola Anna,Auvinen Anssi,Raitanen Jani,Schoemaker Minouk J,Christensen Helle C,Feychting Maria,Johansen Christoffer,Klaeboe Lars,Lönn Stefan,Swerdlow Anthony J,Tynes Tore,Salminen Tiina International journal of cancer Public concern has been expressed about the possible adverse health effects of mobile telephones, mainly related to intracranial tumors. We conducted a population-based case-control study to investigate the relationship between mobile phone use and risk of glioma among 1,522 glioma patients and 3,301 controls. We found no evidence of increased risk of glioma related to regular mobile phone use (odds ratio, OR = 0.78, 95% confidence interval, CI: 0.68, 0.91). No significant association was found across categories with duration of use, years since first use, cumulative number of calls or cumulative hours of use. When the linear trend was examined, the OR for cumulative hours of mobile phone use was 1.006 (1.002, 1.010) per 100 hr, but no such relationship was found for the years of use or the number of calls. We found no increased risks when analogue and digital phones were analyzed separately. For more than 10 years of mobile phone use reported on the side of the head where the tumor was located, an increased OR of borderline statistical significance (OR = 1.39, 95% CI 1.01, 1.92, p trend 0.04) was found, whereas similar use on the opposite side of the head resulted in an OR of 0.98 (95% CI 0.71, 1.37). Although our results overall do not indicate an increased risk of glioma in relation to mobile phone use, the possible risk in the most heavily exposed part of the brain with long-term use needs to be explored further before firm conclusions can be drawn. 10.1002/ijc.22503
    Alcohol consumption and risk of glioma: a meta-analysis of 19 observational studies. Qi Zhen-Yu,Shao Chuan,Yang Chao,Wang Zhong,Hui Guo-Zhen Nutrients The relationship between risk of glioma and alcohol consumption has been widely studied, but results have been conflicting. We therefore conducted a meta-analysis of observational studies to systematically assess the relationship between alcohol drinking and risk of glioma. Two electronic databases (PubMed and EMBASE) were searched from inception to 8 August 2013 to identify pertinent studies that linked alcohol drinking with glioma risk. We used a random-effects model to calculate the overall relative risk (RR) with corresponding 95% confidence intervals (CIs). Fifteen case-control and four cohort studies were identified for this analysis. The combined RR for total alcohol drinkers versus non-drinkers was 0.96 (95% CI: 0.89-1.04). In the subgroup analysis by geographic area, a significant association was observed in North American studies (RR = 0.78, 95% CI: 0.65-0.93), but not in European or Asian/Australian studies. In the subgroup analysis by study design, a borderline significant association emerged in population-based case-control studies (RR = 0.82, 95% CI: 0.68-0.99), but not in hospital-based case-control studies (RR = 1.00, 95% CI: 0.99-1.01) or cohort group (RR = 1.03, 95% CI: 0.88-1.20). Our results show no material association between alcohol consumption and risk of glioma existed. Further prospective evidences are needed to confirm this association. 10.3390/nu6020504
    Pre-diagnostic circulating concentrations of fat-soluble vitamins and risk of glioma in three cohort studies. Yue Yiyang,Creed Jordan H,Cote David J,Stampfer Meir J,Wang Molin,Midttun Øivind,McCann Adrian,Ueland Per Magne,Furtado Jeremy,Egan Kathleen M,Smith-Warner Stephanie A Scientific reports Few prospective studies have evaluated the relation between fat-soluble vitamins and glioma risk. Using three cohorts-UK Biobank (UKB), Nurses' Health Study (NHS), and Health Professionals Follow-Up Study (HPFS), we investigated associations of pre-diagnostic concentrations of fat-soluble vitamins D, A, and E with incident glioma. In 346,785 participants (444 cases) in UKB, associations with vitamin D (25-hydroxyvitamin D [25(OH)D]) were evaluated by Cox proportional hazards regression. In NHS (52 cases, 104 controls) and HPFS (32 cases, 64 controls), associations with 25(OH)D, vitamin A (retinol), and vitamin E (α- and γ-tocopherol) were assessed using conditional logistic regression. Our results suggested plasma concentrations of 25(OH)D and retinol were not associated with glioma risk. Comparing the highest to lowest tertile, the multivariable hazard ratio (MVHR) for 25(OH)D was 0.87 (95% confidence interval [CI] 0.68-1.11) in UKB and the multivariable risk ratio (MVRR) was 0.97 (95% CI 0.51-1.85) in NHS and HPFS. In NHS and HPFS, the MVRR for the same comparison for retinol was 1.16 (95% CI 0.56-2.38). Nonsignificant associations were observed for α-tocopherol (MVRR = 0.61, 95% CI 0.29-1.32) and γ-tocopherol (MVRR  = 1.30, 95% CI 0.63-2.69) that became stronger in 4-year lagged analyses. Further investigation is warranted on a potential association between α- and γ-tocopherol and glioma risk. 10.1038/s41598-021-88485-0
    Older age at the completion of linear growth is associated with an increased risk of adult glioma. Little Rebecca B,Nabors L Burt,Olson Jeffrey J,Thompson Zachary J,Rozmeski Carrie M,LaRocca Renato V,Forsyth Peter A,Thompson Reid C,Oster Robert A,Chowdhary Sajeel A,Egan Kathleen M Cancer causes & control : CCC PURPOSE:To examine the association of age when adult height was attained with glioma risk. METHODS:We analyzed data from a US-based case-control study of glioma risk factors. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) associated between age at attainment of adult height and glioma risk. Multivariate models were adjusted for age, race, sex, education, and state of residence. We examined associations overall, and according to glioma grade, sex, and final adult height. RESULTS:The study set included n = 951 controls and n = 776 cases, with a median age of 56 (18-92); the majority was male (53.8%) and identified as Caucasian. Older age at height completion was associated with an increased risk of glioma. A significant positive trend was observed both for glioblastoma (OR 1.10; 95% CI 1.04-1.17 per 1-year increase in age) and lower grade non-glioblastoma subtypes combined (OR 1.18; 95% CI 1.10-1.28 per year increase in age). The association was observed in men and women, and in all categories of final adult height. CONCLUSIONS:We observed for the first time a positive association between glioma risk and a prolonged adolescent growth phase. Our results suggest a role for factors governing the timing and intensity of growth in adolescence as risk-determining exposures in adult glioma. 10.1007/s10552-017-0871-5
    Anxiety and depression in glioma patients: prevalence, risk factors, and their correlation with survival. Hao Aiping,Huang Junling,Xu Xin Irish journal of medical science AIMS:This study aimed to investigate the risk factors and prognostic value of anxiety and depression in glioma patients. METHODS:A total of 190 glioma patients who underwent resection were consecutively enrolled. Anxiety was assessed using hospital anxiety and depression scale (HADS) and Zung self-rating anxiety scale (SAS); depression was assessed with the use of HADS and Zung self-rating depression scale (SDS). All patients were followed up to death or 36 months. Overall survival (OS) was calculated according to the survival data. RESULTS:The prevalence of anxiety ranged from 36.3 to 37.4%, and the prevalence of depression ranged from 28.4 to 32.6% based on different assessment scales. Female, diabetes, and increased WHO grade were correlated with HADS anxiety and SAS anxiety, while female, single/divorced/widowed status, hyperlipidemia, diabetes, and CKD were associated with HADS depression and SDS depression. Further multivariate logistic analyses disclosed the following: single/divorced/widowed status and WHO grade were independent risk factors for HADS anxiety; female and hyperlipidemia were independent risk factors for SAS anxiety; whereas education duration (< 12 years), single/divorced/widowed status, and CKD were independent risk factors for HADS depression; female, single/divorced/widowed status, and hyperlipidemia were independent risk factors for SDS depression. Besides, HADS anxiety, SAS anxiety and SDS depression were correlated with shorter OS, while HADS depression was not. CONCLUSIONS:Our findings about the risk factors and prognostic value of anxiety and depression might aid for their early prevention and prognosis improvement in glioma patients. 10.1007/s11845-020-02374-5
    A prospective study of dietary flavonoid intake and risk of glioma in US men and women. Bever Alaina M,Cassidy Aedin,Rimm Eric B,Stampfer Meir J,Cote David J The American journal of clinical nutrition BACKGROUND:Flavonoids are a diverse group of plant constituents with demonstrated neuroprotective and anti-tumor effects. Flavonoid intake may decrease the risk of glioma, but the possibility of an association has not yet been investigated in humans. OBJECTIVES:We evaluated the association between dietary flavonoid consumption and the risk of glioma. METHODS:We followed participants in the female Nurses' Health Study (1984-2014; n = 81,688) and Nurses' Health Study II (1991-2017; n = 95,228) and the male Health Professionals Follow-Up Study (1986-2014; n = 49,885). We used multivariable-adjusted Cox proportional hazards regression models to evaluate the associations between average long-term (up to 30 years) or recent (up to 12 years) dietary flavonoid intake (total flavonoids and each of 6 subclasses) and risks of incident glioma. Flavonoid intake was derived from validated quadrennial FFQs. Incident glioma was self-reported and confirmed by a medical record review or was determined by a medical record review after death. RESULTS:We documented 536 incident cases of glioma across 5,936,386 person-years of follow-up. Long-term total flavonoid, flavan-3-ol, and polymeric flavonoid (polymer) intakes were associated with decreased glioma risks in pooled analyses comparing the highest to lowest quintiles of consumption [HR, 0.79 (95% CI, 0.59-1.05; P-trend = 0.04) for total flavonoids; 0.76 (95% CI, 0.57-1.01; P-trend = 0.04) for flavan-3-ols; and 0.82 (95% CI, 0.61-1.09; P-trend = 0.05) for polymers]. Associations with recent intake were weaker. There were no associations with other flavonoid subclasses. After additional adjustment for tea consumption, there were no associations between flavan-3-ol or polymer consumption and glioma. CONCLUSIONS:Increased dietary intakes of flavan-3-ol and polymeric flavonoids, especially those predominant in tea, were associated with decreased glioma risks in a prospective cohort of men and women. 10.1093/ajcn/nqab178
    A prospective study of coffee and tea consumption and the risk of glioma in the UK Biobank. Creed Jordan H,Smith-Warner Stephanie A,Gerke Travis A,Egan Kathleen M European journal of cancer (Oxford, England : 1990) BACKGROUND:Coffee and tea have been hypothesised to reduce the risk of some cancers; however, their impact on glioma is less well studied. METHODS:We examined associations between self-reported intake of tea and coffee in relation to glioma risk in the UK Biobank. We identified 487 incident glioma cases among 379,259 participants. Hazard ratios (HR) and 95% confidence intervals (CI) for glioma according to caffeinated beverage consumption were calculated using Cox proportional hazards regression with adjustment for age, gender, race and education; daily cups of tea or coffee were included in models considering the other beverage. RESULTS:Consuming 4 or more cups of tea was associated with reduced risk of glioma when compared to no tea consumption (HR = 0.69; 95% CI, 0.51-0.94). A significant inverse association was observed for glioblastoma (HR = 0.93 per 1 cup/d increment; 95% CI, 0.89-0.98) and among males for all gliomas combined (HR = 0.95 per 1 cup/d increment; 95% CI, 0.90-1.00). A suggestive inverse association was also observed with greater consumption of coffee (HR = 0.71; 95% CI, 0.49-1.05 for >4 versus 0 cups/d). Results were not materially changed with further adjustment for smoking, alcohol and body mass index. Associations were similar in 2-year and 3-year lagged analyses. CONCLUSIONS:In this prospective study, we found a significant inverse association between tea consumption and the risk of developing glioma, and a suggestive inverse association for the consumption of coffee. Further investigation on the possible preventive role of caffeine in glioma is warranted. 10.1016/j.ejca.2020.01.012
    The impact of body mass index and height on the risk for glioblastoma and other glioma subgroups: a large prospective cohort study. Wiedmann Markus K H,Brunborg Cathrine,Di Ieva Antonio,Lindemann Kristina,Johannesen Tom B,Vatten Lars,Helseth Eirik,Zwart John A Neuro-oncology Background:Glioma comprises a heterogeneous group of mostly malignant brain tumors, whereof glioblastoma (GBM) represents the largest and most lethal subgroup. Body height and body mass index (BMI) are risk factors for other cancers, but no previous study has examined anthropometric data in relation to different glioma subgroups. Methods:This prospective cohort study includes 1.8 million Norwegian women and men between ages 14 and 80 years at baseline. Body weight and height were measured, and incident cases of glioma were identified by linkage to the National Cancer Registry. Cox regression analyses were performed to evaluate risk for different glioma subgroups in relation to anthropometric measures. Results:During 54 million person-years of follow-up, 4,382 gliomas were identified. Overweight and obesity were not associated with risk for any glioma subgroup. Height was positively associated with risk for GBM and all other gliomas (hazard ratio [HR] per 10 cm increase: 1.24; 95% confidence interval [CI], 1.17-1.31 and 1.18; 95% CI, 1.09-1.29) but not with the proxy for isocitrate dehydrogenase (IDH)-mutant glioma (HR, 1.09; 95% CI, 0.98-1.21). In further subgroup analyses, the effect of height on glioma risk varied significantly with positive associations for oligoastrocytoma (HR, 1.74; 95% CI, 1.20-2.53) and malignant glioma not otherwise specified (NOS) (HR, 1.42; 95% CI, 1.16-1.76, but not with diffuse astrocytoma (WHO grades II and III) or oligodendroglioma. Conclusion:This epidemiologic study consolidates height as a risk factor for GBM and other gliomas. It further indicates that this association is not universal for gliomas but may differ between different glioma subgroups. 10.1093/neuonc/now272
    Allergic conditions reduce the risk of glioma: a meta-analysis based on 128,936 subjects. Zhao Hongyu,Cai Weisong,Su Shitao,Zhi Debao,Lu Jie,Liu Shuo Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine Many studies have investigated the association between the allergic conditions and the risk of glioma. However, the evidence is inadequate to draw robust conclusions because most studies were generally small and conducted in heterogeneous populations. To shed light on these inconclusive findings, we conducted a meta-analysis of studies relating the allergic conditions to the risk of glioma. We identified the relevant studies by searching ISI Web of Science, PubMed, EMBASE, Chinese National Knowledge Infrastructure (CNKI) databases, and Wanfang database by October 2013. We included studies that reported odds ratio (OR) or hazard ratio (HR) with its 95% confidence interval (CI) for the association between the allergic condition and the risk of glioma. Eighteen independent publications, with 9,986 glioma cases and 118,950 controls, were included. Our results showed that allergic condition was reversely associated with the risk of glioma (OR = 0.78, 95% CI 0.73-0.83, P < 0.001). The results of our meta-analysis indicated that allergic conditions significantly reduce the risk of glioma. 10.1007/s13277-013-1514-4
    Personal hair dyes use and risk of glioma: a meta-analysis. Shao Chuan,Qi Zhen-Yu,Hui Guo-Zhen,Wang Zhong International journal of clinical and experimental medicine BACKGROUND AND OBJECTIVE:Use of hair dyes for glioma risk has been investigated in numerous epidemiological studies, but the evidence is inconsistent. Therefore, a meta-analysis was performed to estimate the association between hair dyes use and glioma risk. METHODS:We searched PubMed and EMBASE databases without any limitations, covering all papers published by the end of March 8, 2013. Cohort and case-control studies reporting relative risk estimates (RRs) with corresponding 95% confidence intervals (CIs) (or data to calculate them) on this issue were included. Random effects models were used to calculate the pooled RRs and corresponding 95% CIs. RESULTS:Four case-control and two cohort studies were included in this meta-analysis. The summary RRs and 95 % CIs for ever users of any hair dyes were 1.132 (0.887-1.446) for all studies, 1.291 (0.938-1.777) for case-control studies, and 0.903 (0.774-1.054) for cohort studies. In the subgroup analysis by geographic regions and sex, the similar results were detected. No significant associations were also observed among the studies which reported data involving permanent hair dye use and duration of any hair dye use. CONCLUSION:In summary, the results of our study demonstrated that hair dyes use is not associated with risk of glioma.
    Coffee, tea, caffeine intake, and risk of adult glioma in three prospective cohort studies. Holick Crystal N,Smith Scott G,Giovannucci Edward,Michaud Dominique S Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology Current data suggest that caffeinated beverages may be associated with lower risk of glioma. Caffeine has different effects on the brain, some of which could play a role in brain carcinogenesis, and coffee has been consistently associated with reduced risk of liver cancer, thus suggesting a potential anticarcinogenic effect. A total of 335 incident cases of gliomas (men, 133; women, 202) were available from three independent cohort studies. Dietary intake was assessed by food frequency questionnaires obtained at baseline and during follow-up. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between consumption of coffee, tea, carbonated beverages, caffeine, and glioma risk adjusting for age and total caloric intake. Estimates from each cohort were pooled using a random-effects model. Consumption of five or more cups of coffee and tea daily compared with no consumption was associated with a decrease risk of glioma (RR, 0.60; 95% CI, 0.41-0.87; P(trend) = 0.04). Inverse, although weaker, associations were also observed between coffee, caffeinated coffee, tea, and carbonated beverages and glioma risk. No association was observed between decaffeinated coffee and glioma risk. Among men, a statistically significant inverse association was observed between caffeine consumption and risk of glioma (RR, 0.46; 95% CI, 0.26-0.81; P(trend) = 0.03); the association was weaker among women. Our findings suggest that consumption of caffeinated beverages, including coffee and tea, may reduce the risk of adult glioma, but further research is warranted to confirm these findings in other populations. 10.1158/1055-9965.EPI-09-0732
    Cigarette smoking, alcohol intake, and risk of glioma in the NIH-AARP Diet and Health Study. Braganza M Z,Rajaraman P,Park Y,Inskip P D,Freedman N D,Hollenbeck A R,Berrington de González A,Kitahara C M British journal of cancer BACKGROUND:Although cigarette smoking and alcohol drinking increase the risk of several cancers and certain components of cigarette smoke and alcohol can penetrate the blood-brain barrier, it remains unclear whether these exposures influence the risk of glioma. METHODS:We examined the associations between cigarette smoking, alcohol intake, and risk of glioma in the National Institutes of Health-AARP Diet and Health Study, a prospective study of 477,095 US men and women ages 50-71 years at baseline. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using models with age as the time metric and adjusted for sex, race/ethnicity, education, and marital status. RESULTS:During a median 10.5 person-years of follow-up, 492 men and 212 women were diagnosed with first primary glioma. Among men, current, heavier smoking was associated with a reduced risk of glioma compared with never smoking, but this was based on only nine cases. No associations were observed between smoking behaviours and glioma risk in women. Greater alcohol consumption was associated with a decreased risk of glioma, particularly among men (>2 drinks per day vs <1 drink per week: HR=0.67, 95% CI=0.51-0.90). CONCLUSION:Smoking and alcohol drinking do not appear to increase the risk of glioma. 10.1038/bjc.2013.611
    Does smoking increase the risk of developing glioma? A meta-analysis based on case-control studies. Guo Xiaqing,Wang Yabo Journal of cancer research and therapeutics OBJECTIVE:The purpose of this study was to assess the relationship between smoking and glioma risk by meta-analysis. MATERIALS AND METHODS:We have searched the databases of MEDLINE, EMBASE, Ovid, and CNKI to find the suitable studies related to association between smoking and glioma risk. The pooled odds ratio (OR) and 95% confidence interval (CI) of smokers in glioma patients compared to normal controls were aggregated by statistic software Stata11.0. The publication bias was evaluated by Begg's funnel plot. RESULTS:Finally, seven case-control studies were included in this meta-analysis. The pooled results showed that smoking did not increase the risk of glioma (OR = 0.96, 95% CI = 0.86-1.07, P > 0.05). CONCLUSION:No close association between smoking and glioma risk was found in this meta-analysis, which indicate that smoking may not contribute to the incidence of glioma. 10.4103/0973-1482.200758
    Occupational exposure to ionizing and non-ionizing radiation and risk of glioma. Karipidis Ken K,Benke Geza,Sim Malcolm R,Kauppinen Timo,Giles Graham Occupational medicine (Oxford, England) BACKGROUND:Although the aetiology of glioma is poorly understood, the higher incidence in males has long suggested an occupational cause. AIM:To investigate possible associations between occupational exposure to ionizing, ultraviolet (UV), radiofrequency (RF) and extremely low frequency (ELF) radiation and adult glioma risk. METHODS:Case-control study using histologically confirmed cases of glioma first diagnosed between 1987 and 1991 in Melbourne, Australia, matched by age, sex and postcode of residence. A detailed occupational history was obtained for each subject. Exposure to radiation was assessed using a Finnish job exposure matrix (FINJEM) for all the radiation types as well as self-reports and expert hygienist review for RF and ionizing radiation. For ELF and UV, gender-specific FINJEM analysis was performed. RESULTS:The study population consisted of 416 cases of glioma and 422 controls. The risk estimates given by FINJEM for ELF, RF and ionizing radiation were close to or below unity. Gender-specific analysis for UV showed odds ratios of 1.60 [95% confidence interval (CI) 0.95-2.69] and 0.54 (95% CI 0.27-1.07) for the highest exposed group of men and women, respectively (corresponding P value for trend was 0.03 and 0.04). CONCLUSIONS:We did not find evidence of an association between glioma and occupational exposure to ELF, RF and ionizing radiation. UV radiation was associated with increased glioma risk for men but this result could have been confounded by other predominantly male occupational and lifestyle exposures associated with high UV. Further investigation of UV radiation and glioma risk is suggested. 10.1093/occmed/kqm078
    Does diabetes decrease the risk of glioma? A systematic review and meta-analysis of observational studies. Wang Yongbo,Sun Yi,Tang Juan,Zhou Wei,Liu Xiaoxue,Bi Yongyi,Zhang Zhi-Jiang Annals of epidemiology PURPOSE:Increasing epidemiologic evidence suggests that diabetes mellitus (DM) may be associated with a decreased risk of glioma. This systematic review assessed whether DM was associated with glioma risk. METHODS:Electronic searches were performed in PubMed, Web of Science, EMBASE, and Cochrane Library databases up to August 30, 2018. A random-effects model was performed to calculate summary effect size with corresponding 95% confidence intervals (CIs). RESULTS:In total, 10 studies (eight case-control studies and two cohort studies) matched the inclusion criteria. Meta-analyses of case-control studies showed that DM decreased the risk of glioma by 23% (odds ratio: 0.77, 95% CI: 0.61-0.96; P = .02, I = 82.0%). However, no such effect was observed in cohort studies (relative risk: 0.71, 95% CI: 0.10-4.80; P = .72, I = 61.6%). In the subgroup analyses, DM was associated with a decreased risk of glioma in Caucasians but not in Asians; the inverse association was slightly higher in males than in females. CONCLUSIONS:Our results indicate that DM decreases the risk of glioma, but the inverse association may vary in subgroups. The present conclusions should be confirmed with further studies. 10.1016/j.annepidem.2018.11.010
    Use of statins and risk of glioma: a nationwide case-control study in Denmark. Gaist D,Andersen L,Hallas J,Sørensen H Toft,Schrøder H D,Friis S British journal of cancer BACKGROUND:Laboratory studies and a single case-control study have suggested a protective effect of statins on the risk of glioma. We wished to investigate the influence of statin use on the risk of glioma in a population-based setting. METHODS:We conducted a nationwide case-control study in Denmark based on population-based medical registries. We identified all patients aged 20 to 85 years with a first diagnosis of histologically verified glioma during 2000-2009. These cases were matched on birth year and sex with population controls. Prior use of statins since 1995 was classified into short-term use (<5 years) and long-term use (5+ years). We used conditional logistic regression to compute odds ratios (ORs), with 95% confidence intervals (CIs), for glioma associated with statin use, adjusted for potential confounders. RESULTS:A total of 2656 cases and 18,480 controls were included in the study. The risk of glioma was reduced among long-term statin users (OR=0.76; 95% CI: 0.59-0.98) compared with never users of statins, and was inversely related to the intensity of statin treatment among users (OR=0.71; 95% CI: 0.44-1.15 for highest intensity). The inverse association between long-term statin treatment and glioma risk was more pronounced among men aged ≤ 60 years (OR=0.40; 95% CI: 0.17-0.91) compared with men aged 60+ years (OR=0.71; 95% CI: 0.49-1.03). An inverse association was also observed among women aged ≤ 60 years (OR=0.28; 95% CI: 0.06-1.25), but not among women over age 60 years (OR=1.23; 95% CI: 0.82-1.85). CONCLUSION:Long-term statin use may reduce the risk of glioma. 10.1038/bjc.2012.536
    Association of Rosacea With Risk for Glioma in a Danish Nationwide Cohort Study. Egeberg Alexander,Hansen Peter R,Gislason Gunnar H,Thyssen Jacob P JAMA dermatology IMPORTANCE:Rosacea, a common facial skin disorder, has a poorly understood pathogenesis in which increased matrix metalloproteinase activity might play an important role. Glioma accounts for 80% of all primary malignant tumors in the central nervous system, and these tumors also show upregulation of certain matrix metalloproteinases. OBJECTIVE:To investigate the association between rosacea and the risk for glioma. DESIGN, SETTING, AND PARTICIPANTS:Nationwide cohort study of the Danish population from individual-level linkage of administrative registers. All Danish citizens 18 years or older from January 1, 1997, to December 31, 2011, were eligible for inclusion. A total of 5 484 910 individuals were eligible for analysis; of these, 68 372 had rosacea and 5 416 538 constituted the reference population. Data were analyzed from July 14 to August 10, 2015. MAIN OUTCOMES AND MEASURES:The outcome of interest was a diagnosis of glioma. Incidence rates per 10 000 person-years were calculated, and incidence rate ratios adjusted for age, sex, and socioeconomic status were estimated by Poisson regression distribution models. RESULTS:Of the 5 484 910 individuals in the study population, 21 118 individuals developed glioma during the study period, including 20 934 of the 5 416 538 individuals in the reference population (50.4% women; mean [SD] age, 40.8 [19.7] years) and 184 of the 68 372 patients with rosacea (67.3% women; mean [SD] age, 42.2 [16.5] years). The incidence rate (95% CI) of glioma was 3.34 (3.30-3.39) in the reference population and 4.99 (4.32-5.76) in patients with rosacea. The adjusted incidence rate ratio (95% CI) of glioma in patients with rosacea was 1.36 (1.18-1.58) in our primary analysis. When analyses were limited to patients with a primary diagnosis of rosacea by a hospital dermatologist (n = 5964), the adjusted incidence rate ratio was 1.82 (1.16-2.86). CONCLUSIONS AND RELEVANCE:Rosacea was associated with a significantly increased risk for glioma in a nationwide cohort. This association may be mediated, in part, by mechanisms dependent on matrix metalloproteinases. Increased focus on neurologic symptoms in patients with rosacea may be warranted. 10.1001/jamadermatol.2015.5549
    Diet and risk of adult glioma in eastern Nebraska, United States. Chen Honglei,Ward Mary H,Tucker Katherine L,Graubard Barry I,McComb Rodney D,Potischman Nancy A,Weisenburger Dennis D,Heineman Ellen F Cancer causes & control : CCC OBJECTIVE:To investigate potential associations between diet and adult glioma. METHODS:We conducted a population-based case-control study of adult glioma in eastern Nebraska. Nutrient and food group intakes were estimated for 236 glioma cases and 449 controls using information obtained from a food-frequency questionnaire. RESULTS:After adjusting for potential confounders, inverse associations with risk of adult glioma were observed for intakes of dark yellow vegetables (highest quartile versus lowest: OR = 0.6, Ptrend = 0.03) and beans (OR = 0.4, Ptrend = 0.0003), but no associations were seen for dietary sources of preformed nitrosamines or high-nitrate vegetables. Our nutrient analysis revealed significant inverse associations between risk of adult glioma and dietary intake of pro-vitamin A carotenoids (highest quartile versus lowest: OR = 0.5, Ptrend = 0.005), a-carotene (OR = 0.5, Ptrend = 001), beta-carotene (OR = 0.5, Ptrend = 0.01), dietary fiber (OR=0.6, Ptrend = 0.048) and fiber from beans (OR = 0.5, Ptrend = 0.0002). We observed no significant associations with risk of adult glioma for intakes of other nutrients or compounds including nitrate, nitrite, vitamin C, vitamin E, saturated fat, cholesterol, dietary fiber from grain products, or fiber from fruit and vegetables. CONCLUSION:Our study does not support the N-nitroso compound hypothesis, but suggests potential roles for carotenoids and possibly other phytochemicals in reducing risk of adult glioma. 10.1023/a:1019527225197
    Pediatric glioma and medulloblastoma risk and population demographics: a Poisson regression analysis. Muskens Ivo S,Feng Qianxi,Francis Stephen S,Walsh Kyle M,Mckean-Cowdin Roberta,Gauderman William J,de Smith Adam J,Wiemels Joseph L Neuro-oncology advances Background:The incidence of pediatric brain tumors varies by race and ethnicity, but these relationships may be confounded by socioeconomic status (SES). In this study, the Surveillance, Epidemiology, and End Results Program (SEER) database was evaluated for associations between race/ethnicity and pediatric glioma and medulloblastoma risk with adjustment for SES. Methods:Pediatric glioma and medulloblastoma cases from the SEER database (years: 2000-2016) were included. Differences in incidence rates by ethnicity, sex, age, and SES-related factors were evaluated by calculation of age-adjusted incidence rates (AAIRs) and annual percent change (APC). SES-related factors (percentage without less than high school graduation, median household income, and percentage foreign-born) were derived from the census at the county-level (year: 2000). Multivariable Poisson regression models with adjustment for selected covariates were constructed to evaluate risk factors. Results:The highest AAIRs of pediatric glioma were observed among non-Hispanic Whites (AAIR: 2.91 per 100 000, 95%-CI: 2.84-2.99). An increasing incidence of pediatric glioma by calendar time was observed among non-Hispanic Whites and non-Hispanic Blacks (APC: 0.97%, 95%-CI: 0.28-1.68 and APC: 1.59%, 95%-CI: 0.03-3.18, respectively). Hispanic and non-Hispanic Black race/ethnicity was associated with lower risk when compared with non-Hispanic White (incidence rate ratios [IRRs]: 0.66, 95%-CI: 0.63-0.70; and 0.69, 95%-CI: 0.65-0.74, respectively). For medulloblastoma, the highest AAIR was observed for non-Hispanic Whites with a positive APC (1.52%, 95%-CI: 0.15-2.91). Hispanics and non-Hispanic Blacks had statistically significant lower IRRs compared with non-Hispanic Whites (IRRs: 0.83, 95%-CI: 0.73-0.94; and 0.72, 95%-CI: 0.59-0.87, respectively). Conclusion:Non-Hispanic White race/ethnicity was associated with higher pediatric glioma and medulloblastoma IRRs in models with adjustments for SES. 10.1093/noajnl/vdaa089
    Coffee and tea consumption and the risk of glioma: a systematic review and dose-response meta-analysis. Pranata Raymond,Feraldho Andrea,Lim Michael Anthonius,Henrina Joshua,Vania Rachel,Golden Nyoman,July Julius The British journal of nutrition In this systematic review and dose-response meta-analysis, we aimed to assess whether coffee and tea consumption is related to the risk of glioma. We performed a systematic literature search using PubMed, Embase, Scopus and the EuropePMC from the inception of database up until 1 October 2020. Exposures in the present study were coffee and tea consumption, the main outcome was the incidence of glioma. The present study compares the association between the exposure of coffee and tea with the incidence of glioma, and the results are reported in relative risks (RR). There are 12 unique studies comprising of 1 960 731 participants with 2987 glioma cases. Higher coffee consumption was associated with a statistically non-significant trend towards lower risk of glioma (RR 0·77 (95 % CI 0·55, 1·03), P= 0·11; I2:75·27 %). Meta-regression showed that the association between coffee and glioma was reduced by smoking (P= 0·029). Higher tea consumption was associated with a lower risk of glioma (RR 0·84 (95 % CI 0·71, 0·98), P= 0·030; I2:16·42 %). Sensitivity analysis by removal of case-control studies showed that higher coffee consumption (RR 0·85 (95 % CI 0·72, 1·00), P= 0·046; I2:0 %) and higher tea consumption (RR 0·81 (95 % CI 0·70, 0·93), P= 0·004; I2:0 %, Pnon-linearity = 0·140) were associated with lower risk of glioma. Dose-response meta-analysis showed that every one cup of coffee per day decreases the risk of glioma by 3 % (RR 0·97 (95 % CI 0·94, 0·99), P= 0·016, Pnon-linearity = 0·054) and every one cup of tea per day decreases the risk of glioma by 3 % (RR 0·97 (95 % CI 0·94, 1·00), P= 0·048). This meta-analysis showed apparent association between coffee and tea intake and risk of glioma. 10.1017/S0007114521000830
    Hormonal and reproductive factors and risk of glioma: a prospective cohort study. Silvera Stephanie A Navarro,Miller Anthony B,Rohan Thomas E International journal of cancer The etiology of glioma, the most commonly diagnosed malignant brain tumor among adults in the United States, is poorly understood. Given the lower incidence rate of glioma in women than in men, it has been hypothesized that reproductive and hormonal factors may be involved in the etiology of glioma. We conducted a secondary analysis of data from the National Breast Screening Study, which included 89,835 Canadian women, aged 40-59 years at recruitment between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths from all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals (CI) for the association between hormonal and reproductive factors and risk of glioma. During a mean of 16.4 years of follow-up, we observed 120 incident glioma cases. Compared with women with a relatively early age at menarche (< or =12 years), women who were 13-14 years of age at menarche had a 64% increased risk of glioma (95% CI = 1.01-2.65), and women who were older than 14 years of age at menarche had a 66% increased risk of glioma (95% CI = 0.86-3.20, p(trend) = 0.06). Age at first live birth, parity, menopausal status, use of oral contraceptive and use of hormone replacement therapy were not associated with altered glioma risk in our study population. Additional prospective studies are needed to confirm our findings. 10.1002/ijc.21467
    Hair dyes and risk of glioma among Nebraska women. Heineman Ellen F,Ward Mary H,McComb Rodney D,Weisenburger Dennis D,Zahm Shelia Hoar Cancer causes & control : CCC The etiology of brain cancer is not well understood. We conducted a population-based case-control study among 112 white women in Nebraska who were newly diagnosed with glioma between July 1988 and June 1993, and 215 controls, to identify risk factors for this disease. A 1.7-fold increased risk of glioma was observed for women who ever used hair coloring products (95% confidence interval (CI) = 1.0-2.9, 62 cases), and a 2.4-fold risk for those who used permanent hair coloring products (odds ratio (OR) = 2.4, 95% CI = 1.3-4.5, 39 cases). For women with the most aggressive form of glioma, glioblastoma multiforme, risk increased with duration of exposure to 4.9 (95% CI = 1.6-15.7, 10 cases) after 21 or more years of permanent hair coloring use. Higher risks were observed with earlier age at first use, but we did not see an exposure-response pattern with frequency of use of permanent dyes. No association was observed with use of non-permanent (sometimes called temporary or semi-permanent) hair coloring products. These suggestive findings need confirmation in future studies with larger sample sizes, fewer proxy respondents, and the ability to evaluate the effect of changes in formulations over time. 10.1007/s10552-005-3204-z
    Cancer in first-degree relatives and risk of glioma in adults. Hill Deirdre A,Inskip Peter D,Shapiro William R,Selker Robert G,Fine Howard A,Black Peter M,Linet Martha S Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology Relatively few studies have examined glioma risk in relation to history of cancer in first-degree relatives. We sought to describe such risks in a large hospital-based case-control study. Histologically confirmed incident adult glioma cases (n = 489) were identified at three regional referral hospitals between June 1994 and August 1998. Controls (n = 799) admitted to the same hospitals for nonmalignant conditions were frequency-matched on age, sex, race/ethnicity, hospital, and proximity of residence to hospital. Participants received a personal interview, including questions regarding cancer in family members. Odds ratios (ORs) were calculated to estimate the risk of glioma associated with a history of cancer in a first-degree relative using conditional logistic regression and compared with standardized incidence ratios among relatives of cases versus relatives of controls. Among participants reporting a family history of a brain cancer or a brain tumor, risk of glioma was 1.6 [95% confidence interval (CI), 0.5-5.3; n = 5] and 3.0 (95% CI, 0.9-10.8; n = 7), respectively, in comparison with those without such family histories. Participants who had a family history of stomach (OR, 2.2; 95% CI, 1.0-4.6), colon (OR, 1.4; 95% CI, 0.9-2.2), or prostate cancer (OR, 2.1; 95% CI, 1.1-3.8) or Hodgkin disease (OR, 2.4; 95% CI, 0.9-6.3) had an increased glioma risk. OR estimates were similar to the ratios of standardized incidence ratios for cancer in relatives of cases versus controls. Shared environmental or genetic factors in families may influence glioma risk. Our findings suggest that individuals with a family history of specific cancers other than glioma may have an increased glioma risk.
    Risk of cancer among relatives of patients with glioma. O'Neill Brian P,Blondal Hannes,Yang Ping,Olafsdottir Gurri H,Sigvaldason H,Jenkins Robert B,Kimmel David W,Scheithauer Bernd W,Rocca Walter A,Bjornsson Johannes,Tulinius Hfran Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology We report a population-based, retrospective study of 396 Icelandic people diagnosed with glioma in the years 1940-1995. The purpose of this study was to test whether astrocytomas, other glial tumors, other central nervous system tumors, or other cancers aggregate in families identified through glioma probands who were of Icelandic origin. Pedigrees of the 396 cases were traced by the Genetical Committee of the University of Iceland and linked to the Icelandic Cancer Registry. A total of 25,546 relatives, including 2,080 individuals with cancer were identified within these pedigrees. There was no statistically significant increase of glioma in relatives of glioma patients, nor was there any statistically significant increase in risk for other central nervous system tumors. There was no overall increase in incidence of all cancer combined, nor of specific common cancers (lung, prostate, breast, stomach, and colorectal) and uncommon cancers (melanoma and pancreas) in the relatives of glioma patients. Our results do not support the hypothesis of a familial aggregation of glioma indicative of a glioma susceptibility gene.
    Body mass index, physical activity, and risk of adult meningioma and glioma: A meta-analysis. Niedermaier Tobias,Behrens Gundula,Schmid Daniela,Schlecht Inga,Fischer Beate,Leitzmann Michael F Neurology OBJECTIVE:Whether adiposity and lack of physical activity affect the risk for developing meningioma and glioma is poorly understood. Our objective was to characterize these associations in detail. METHODS:We conducted a systematic review and meta-analysis of adiposity and physical activity in relation to meningioma and glioma using cohort and case-control studies published through February 2015. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. RESULTS:We identified 12 eligible studies of body mass index (BMI) and 6 studies of physical activity, comprising up to 2,982 meningioma cases and 3,057 glioma cases. Using normal weight as the reference group, overweight (summary relative risk [RR] = 1.21, 95% confidence interval [CI] = 1.01-1.43) and obesity (RR = 1.54, 95% CI = 1.32-1.79) were associated with increased risk of meningioma. In contrast, overweight (RR = 1.06, 95% CI = 0.94-1.20) and obesity (RR = 1.11, 95% CI = 0.98-1.27) were unrelated to glioma. Similarly, dose-response meta-analyses revealed a statistically significant positive association of BMI with meningioma, but not glioma. High vs low physical activity levels showed a modest inverse relation to meningioma (RR = 0.73, 95% CI = 0.61-0.88) and a weak inverse association with glioma (RR = 0.86, 95% CI = 0.76-0.97). Relations persisted when the data were restricted to prospective studies, except for the association between physical activity and glioma, which was rendered statistically nonsignificant (RR = 0.91, 95% CI = 0.77-1.07). CONCLUSIONS:Adiposity is related to enhanced risk for meningioma but is unassociated with risk for glioma. Based on a limited body of evidence, physical activity is related to decreased risk of meningioma but shows little association with risk of glioma. 10.1212/WNL.0000000000002020
    Joint associations between genetic variants and reproductive factors in glioma risk among women. Wang Sophia S,Hartge Patricia,Yeager Meredith,Carreón Tania,Ruder Avima M,Linet Martha,Inskip Peter D,Black Amanda,Hsing Ann W,Alavanja Michael,Beane-Freeman Laura,Safaiean Mahboobeh,Chanock Stephen J,Rajaraman Preetha American journal of epidemiology In a pooled analysis of 4 US epidemiologic studies (1993-2001), the authors evaluated the role of 5 female reproductive factors in 357 women with glioma and 822 controls. The authors further evaluated the independent association between 5 implicated gene variants and glioma risk among the study population, as well as the joint associations of female reproductive factors (ages at menarche and menopause, menopausal status, use of oral contraceptives, and menopausal hormone therapy) and these gene variants on glioma risk. Risk estimates were calculated as odds ratios and 95% confidence intervals that were adjusted for age, race, and study. Three of the gene variants (rs4295627, a variant of CCDC26; rs4977756, a variant of CDKN2A and CDKN2B; and rs6010620, a variant of RTEL1) were statistically significantly associated with glioma risk in the present population. Compared with women who had an early age at menarche (<12 years of age), those who reported menarche at 12-13 years of age or at 14 years of age or older had a 1.7-fold higher risk and a 1.9-fold higher risk of glioma, respectively (P for trend = 0.009). Postmenopausal women and women who reported ever having used oral contraceptives had a decreased risk of glioma. The authors did not observe joint associations between these reproductive characteristics and the implicated glioma gene variants. These results require replication, but if confirmed, they would suggest that the gene variants that have previously been implicated in the development of glioma are unlikely to act through the same hormonal mechanisms in women. 10.1093/aje/kwr184
    Vitamin E intake is not associated with glioma risk: evidence from a meta-analysis. Qin Shiyong,Wang Minghai,Zhang Tao,Zhang Shuguang Neuroepidemiology BACKGROUND:Epidemiological studies evaluating the association between vitamin E intake and glioma risk have produced inconsistent results. Thus, we conducted a meta-analysis to summarize the evidence from epidemiological studies of vitamin E intake with the risk of glioma. METHODS:Pertinent studies were identified by a search in pubmed and web of knowledge up to August 2014. The random-effect model was used to combine the results. Publication bias was estimated using the Egger's regression asymmetry test. RESULTS:Twelve studies including 3180 glioma cases about vitamin E intake with the risk of glioma were included in this meta-analysis. The combined relative risk (RR) of glioma associated with vitamin E intake was 0.88 (95% CI = 0.69-1.12). The association was significant neither in the case-control studies nor in the cohort studies. No publication biases were found. CONCLUSIONS:Our analysis indicated that vitamin E intake is not associated with the risk of glioma. 10.1159/000369345
    Smoking and Glioma Risk: Evidence From a Meta-Analysis of 25 Observational Studies. Shao Chuan,Zhao Wei,Qi Zhenyu,He Jiaquan Medicine To systematically assess the relationship between smoking and glioma risk.A dose-response meta-analysis of case-control and cohort studies was performed. Pertinent studies were identified by searching database and reference lists. Random-effects model was employed to pool the estimates of the relative risks (RRs) with corresponding 95% confidence intervals (CIs).A total of 19 case-control and 6 cohort studies were included. Overall, compared with those who never smoked, the pooled RR and 95% CI was 0.98 (0.92-1.05) for ever smoker. The subgroups were not significantly different regarding risk of glioma except the group of age at start smoking (RR = 1.17, 95% CI: 0.93-1.48 for age < 20; RR = 1.25, 95% CI: 1.02-1.52 for age ≥ 20). Dose-response analysis also suggested no significant association between smoking and the risk of glioma, although some evidence for a linear relationship between smoking and glioma risk was observed.In conclusion, this meta-analysis provides little support for a causal relationship between smoking and risk of glioma. 10.1097/MD.0000000000002447
    Allergic conditions and risk of glioma and meningioma in the CERENAT case-control study. Pouchieu Camille,Raherison Chantal,Piel Clément,Migault Lucile,Carles Camille,Fabbro-Perray Pascale,Loiseau Hugues,Guillamo Jean-Sébastien,Lebailly Pierre,Baldi Isabelle Journal of neuro-oncology Inverse association between allergic conditions and glioma risk has been consistently reported in epidemiological studies with little attention paid to potential environmental confounders; the association with meningioma risk is less consistent. We examined the association between allergy history and risk of glioma and meningioma in adults using data from the CERENAT (CEREbral tumors: a NATional study) multicenter case-control study carried out in 4 areas in France in 2004-2010. Participants' histories of doctor-diagnosed allergic asthma, eczema, rhinitis/hay fever and other allergic conditions were collected at onset through a detailed questionnaire delivered in a face-to-face interview. Conditional logistic regression for matched sets was adjusted for participants' educational level and mobile phone use. A total of 273 glioma cases, 218 meningioma cases and 982 matched controls selected from the local electoral rolls were analyzed. A significant inverse association was found between glioma and a history of any allergy (OR 0.52, 95% CI 0.36-0.75), with a dose-effect relationship with the number of allergic conditions reported (p-trend = 0.001) and a particularly strong association with hay fever/allergic rhinitis (OR 0.46, 95% CI 0.30-0.72). Interestingly, associations with glioma risk were more pronounced in women. For meningioma, no association was observed with overall or specific allergic conditions. Our findings confirmed the inverse association between allergic conditions and glioma risk but questioned the role of allergy in meningioma risk. Future research is needed to clarify the biological mechanism of overall allergy and allergic rhinitis on glioma and to confirm the different effect by gender. 10.1007/s11060-018-2816-6
    Association between fruit and vegetable intake and risk for glioma: a meta-analysis. Li Ying Nutrition (Burbank, Los Angeles County, Calif.) OBJECTIVE:Epidemiologic studies evaluating the association between the intake of vegetables and fruit and the risk for glioma have produced inconsistent results. Therefore, the aim of this study was to test the hypothesis that higher vegetable and fruit intake may have a protective effect on risk for glioma. METHODS:Pertinent studies were identified by a search in PubMed, Web of Knowledge, and Wan Fang Med Online up to January 2014. Random-effect model was used to combine study-specific results. Publication bias was estimated using Begg's funnel plot and Egger's regression asymmetry test. RESULTS:Fifteen studies involving 5562 cases focusing on vegetable intake and 17 studies involving 3994 cases of fruit intake compared with the risk for glioma were included in this meta-analysis. The combined relative risk (RR) of glioma associated with vegetable intake was 0.775 (95% confidence interval [CI], 0.688-0.872) overall, and the association for subgroup analysis by study design, sources of control, ethnicity, and number of cases was consistent with overall data. For fruit intake and glioma risk, significant protective associations were found in an Asian population (RR, 0.573; 95% CI, 0.346-0.947), but not in a white population. No publication bias was found. CONCLUSIONS:This analysis indicated that intake of vegetables might have a protective effect on glioma. The intake of fruit might have a protective effect on glioma in the Asian population; however, the results need to be confirmed. 10.1016/j.nut.2014.03.027
    Toxoplasma gondii infection and the risk of adult glioma in two prospective studies. Hodge James M,Coghill Anna E,Kim Youngchul,Bender Noemi,Smith-Warner Stephanie A,Gapstur Susan,Teras Lauren R,Grimsrud Tom K,Waterboer Tim,Egan Kathleen M International journal of cancer Toxoplasma gondii (T gondii) is a common parasite that shows affinity to neural tissue and may lead to the formation of cysts in the brain. Previous epidemiologic studies have suggested an association between glioma and increased prevalence of T gondii infection, but prospective studies are lacking. Therefore, we examined the association between prediagnostic T gondii antibodies and risk of glioma in two prospective cohorts using a nested case-control study design. Cases and matched controls were selected from the American Cancer Society's Cancer Prevention Study-II Nutrition Cohort (CPSII-NC) (n = 37 cases and 74 controls) and the Norwegian Cancer Registry's Janus Serum Bank (Janus) (n = 323 cases and 323 controls). Blood samples collected prior to diagnosis were analyzed for antibodies to two T gondii surface antigens (p22 and sag-1), with individuals considered seropositive if antibodies to either antigen were detected. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI) for each cohort. In both cohorts, a suggestive increase in glioma risk was observed among those infected with T gondii (OR: 2.70; 95% CI: 0.96-7.62 for CPSII-NC; OR: 1.32, 95% CI: 0.85-2.07 for Janus), particularly among participants with high antibody titers specific to the sag-1 antigen (CPSII-NC OR: 3.35, 95% CI: 0.99-11.38; Janus OR: 1.79, 95% CI: 1.02-3.14). Our findings provide the first prospective evidence of an association between T gondii infection and risk of glioma. Further studies with larger case numbers are needed to confirm a potential etiologic role for T gondii in glioma. 10.1002/ijc.33443
    Height, body mass index, and physical activity in relation to glioma risk. Moore Steven C,Rajaraman Preetha,Dubrow Robert,Darefsky Amy S,Koebnick Corinna,Hollenbeck Albert,Schatzkin Arthur,Leitzmann Michael F Cancer research Whether energy balance during early life and/or adulthood is related to glioma risk is unknown. We therefore investigated height, body mass index (BMI), and physical activity in relation to glioma risk in the prospective NIH-AARP Diet and Health Study. Participants completed a baseline questionnaire (sent in 1995-1996) inquiring about height, weight, and potential confounders. A second questionnaire (sent in 1996) inquired about physical activity during ages 15 to 18, 19 to 29, and 35 to 39 years and the past 10 years and body weight at ages 18, 35, and 50 years. During follow-up from 1995/1996 to 2003, we documented 480 cases of glioma among 499,437 respondents to the baseline questionnaire and 257 cases among 305,681 respondents to the second questionnaire. Glioma risk among tall persons (>or=1.90 m) was twice that of short persons [<1.60 m; multivariate relative risk (RR), 2.12; 95% confidence interval (95% CI), 1.18-3.81; P(trend) = 0.006]. Risk among participants who were obese (BMI 30.0-34.9 kg/m(2)) at age 18 years was nearly four times that of persons of normal weight (BMI 18.5-24.9 kg/m(2)) at age 18 years (RR, 3.74; 95% CI, 2.03-6.90; P(trend) = 0.003); 11 cases were obese at age 18 years. Risk among participants who were active during ages 15 to 18 years was 36% lower than that of persons who were inactive during ages 15 to 18 years (RR, 0.64; 95% CI, 0.44-0.93; P(trend) = 0.02). BMI and physical activity after age 18 years were unrelated to glioma risk. Adult height, BMI during adolescence, and physical activity during adolescence were each associated with glioma risk, supporting a role for early-life energy balance in glioma carcinogenesis. 10.1158/0008-5472.CAN-09-1669
    Association between vitamin C intake and glioma risk: evidence from a meta-analysis. Zhou Siru,Wang Xiaoya,Tan Ya,Qiu Lingli,Fang Huan,Li Wei Neuroepidemiology BACKGROUND:The field of quantifying the association between the intake of vitamin C and risk of glioma still has conflicts. Thus, we performed a comprehensive meta-analysis to test the hypothesis that a high intake of vitamin C may be a protective effect on glioma risk. METHODS:Pertinent studies were identified by a search in PubMed and Web of Knowledge up to June 2014. The random-effect model was used to combine study-specific results. Publication bias was estimated using Begg' funnel plot and Egger's regression asymmetry test. RESULTS:Thirteen articles with 15 studies (2 cohort study and 13 case-control studies) involving 3,409 glioma cases about vitamin C intake and glioma risk were used in this meta-analysis. The combined relative risks (RRs) of glioma associated with vitamin C intake was 0.86 (95% CIs = 0.75-0.99). Overall, significant protective associations were also found in the American population (RRs = 0.85, 95% CIs = 0.73-0.98) and case-control studies (RRs = 0.80, 95% CIs = 0.69-0.93). No publication bias was found. CONCLUSIONS:Our analysis indicated that vitamin C intake might decrease the risk of glioma, especially among the Americans. 10.1159/000369814
    Mendelian randomisation study of the relationship between vitamin D and risk of glioma. Takahashi Hannah,Cornish Alex J,Sud Amit,Law Philip J,Kinnersley Ben,Ostrom Quinn T,Labreche Karim,Eckel-Passow Jeanette E,Armstrong Georgina N,Claus Elizabeth B,Il'yasova Dora,Schildkraut Joellen,Barnholtz-Sloan Jill S,Olson Sara H,Bernstein Jonine L,Lai Rose K,Schoemaker Minouk J,Simon Matthias,Hoffmann Per,Nöthen Markus M,Jöckel Karl-Heinz,Chanock Stephen,Rajaraman Preetha,Johansen Christoffer,Jenkins Robert B,Melin Beatrice S,Wrensch Margaret R,Sanson Marc,Bondy Melissa L,Turnbull Clare,Houlston Richard S Scientific reports To examine for a causal relationship between vitamin D and glioma risk we performed an analysis of genetic variants associated with serum 25-hydroxyvitamin D (25(OH)D) levels using Mendelian randomisation (MR), an approach unaffected by biases from confounding. Two-sample MR was undertaken using genome-wide association study data. Single nucleotide polymorphisms (SNPs) associated with 25(OH)D levels were used as instrumental variables (IVs). We calculated MR estimates for the odds ratio (OR) for 25(OH)D levels with glioma using SNP-glioma estimates from 12,488 cases and 18,169 controls, using inverse-variance weighted (IVW) and maximum likelihood estimation (MLE) methods. A non-significant association between 25(OH)D levels and glioma risk was shown using both the IVW (OR = 1.21, 95% confidence interval [CI] = 0.90-1.62, P = 0.201) and MLE (OR = 1.20, 95% CI = 0.98-1.48, P = 0.083) methods. In an exploratory analysis of tumour subtype, an inverse relationship between 25(OH)D levels and glioblastoma (GBM) risk was identified using the MLE method (OR = 0.62, 95% CI = 0.43-0.89, P = 0.010), but not the IVW method (OR = 0.62, 95% CI = 0.37-1.04, P = 0.070). No statistically significant association was shown between 25(OH)D levels and non-GBM glioma. Our results do not provide evidence for a causal relationship between 25(OH)D levels and all forms of glioma risk. More evidence is required to explore the relationship between 25(OH)D levels and risk of GBM. 10.1038/s41598-018-20844-w
    Wireless Phone Use and Risk of Adult Glioma: Evidence from a Meta-Analysis. Wang Peng,Hou Chongxian,Li Yanwen,Zhou Dong World neurosurgery BACKGROUND:Wireless phone use has been increasing rapidly and is associated with the risk of glioma. Many studies have been conducted on this association without reaching agreement. The aim of this meta-analysis was to determine the possible association between wireless phone use and risk of adult glioma. METHODS:Eligible studies were identified by searching PubMed and Embase up to July 2017. Random-effects or fixed-effects model was used to combine the results depending on the heterogeneity of the analysis. Publication bias was evaluated using Begg's funnel plot and Egger's regression asymmetry test. Subgroup analysis was performed to evaluate possible influence of these variables. RESULTS:Ten studies on the association of wireless phone use and risk of glioma were included. The combined odds ratio of adult gliomas associated with ever use of wireless phones was 1.03 (95% confidence interval [CI], 0.92-1.16) with high heterogeneity (I = 54.2%, P = 0.013). In subgroup analyses, no significant association was found between tumor location in the temporal lobe and adult glioma risk, with odds ratios of 1.26 (95% CI, 0.87-1.84), 0.93 (95% CI, 0.69-1.24), and 1.61 (95% CI, 0.78-3.33). A significant association with risk of glioma was found in long-term users (≥10 years) with odds ratio of 1.33 (95% CI, 1.05-1.67). CONCLUSIONS:Ever use of wireless phones was not significantly associated with risk of adult glioma, but there could be increased risk in long-term users. 10.1016/j.wneu.2018.04.122
    Height, waist circumference, body mass index, and body somatotype across the life course and risk of glioma. Cote David J,Downer Mary K,Smith Timothy R,Smith-Warner Stephanie A,Egan Kathleen M,Stampfer Meir J Cancer causes & control : CCC PURPOSE:Recent studies have suggested height as a risk factor for glioma, but less is known regarding body mass index (BMI) or other anthropomorphic measures. We evaluated the association between body habitus and risk of glioma. METHODS:We evaluated the association of measures of height, BMI, waist circumference, and somatotypes with risk of glioma in two prospective cohorts, the Nurses' Health Study and the Health Professionals Follow-Up Study. RESULTS:We documented 508 incident cases of glioma (321 glioblastoma [GBM]). In both cohorts, we found no significant association between adult BMI or waist circumference and risk of glioma, with pooled HR for BMI of 1.08 (95% CI 0.85-1.38 comparing ≥ 30 to < 25 kg/m) and for waist circumference of 1.05 (95% CI 0.80-1.37 highest vs. lowest quintile). Higher young adult BMI (at age 18 in NHS and 21 in HPFS) was associated with modestly increased risk of glioma in the pooled cohorts (pooled HR 1.35, 95% CI 1.06-1.72 comparing ≥ 25 kg/m vs. less; HR 1.34 for women and 1.37 for men). Analysis of body somatotypes suggested reduced risk of glioma among women with heavier body types at all ages this measure was assessed (HRs ranging from 0.52 to 0.65 comparing highest tertile to lowest tertile), but no significant association among men. Height was associated with increased risk of glioma among women (HR 1.09, 95% CI 1.04-1.14 per inch), but not significantly among men. Within the 8 years prior to diagnosis, cases had no material weight loss compared to non-cases. All results were similar when limited to GBM. CONCLUSION:Adult BMI and waist circumference were not associated with glioma. Higher BMI at age 21 for men and at age 18 for women was modestly associated with risk in the pooled cohort. Based on body somatotypes, however, women with heavier body types during childhood and young adulthood may be at lower risk of glioma, although this association was not observed later in life with measurements of BMI. Greater height was associated with increased risk, and the trend was more pronounced in women. 10.1007/s10552-018-1052-x
    Establishment of age group classification for risk stratification in glioma patients. Lin Zhiying,Yang Runwei,Li Kaishu,Yi Guozhong,Li Zhiyong,Guo Jinglin,Zhang Zhou,Junxiang Peng,Liu Yawei,Qi Songtao,Huang Guanglong BMC neurology BACKGROUND:Age is associated with the prognosis of glioma patients, but there is no uniform standard of age-group classification to evaluate the prognosis of glioma patients. In this study, we aimed to establish an age group classification for risk stratification in glioma patients. METHODS:1502 patients diagnosed with gliomas at Nanfang Hospital between 2000 and 2018 were enrolled. The WHO grade of glioma was used as a dependent variable to evaluate the effect of age on risk stratification. The evaluation model was established by logistic regression, and the Akaike information criterion (AIC) value of the model was used to determine the optimal cutoff points for age-classification. The differences in gender, WHO grade, pathological subtype, tumor cell differentiation, tumor size, tumor location, and molecular markers between different age groups were analyzed. The molecular markers included GFAP, EMA, MGMT, P53, NeuN, Oligo2, EGFR, VEGF, IDH1, Ki-67, PR, CD3, H3K27M, TS, and 1p/19q status. RESULTS:The proportion of men with glioma was higher than that of women with glioma (58.3% vs 41.7%). Analysis of age showed that appropriate classifications of age group were 0-14 years old (pediatric group), 15-47 years old (youth group), 48-63 years old (middle-aged group), and ≥ 64 years old (elderly group).The proportions of glioblastoma and large tumor size (4-6 cm) increased with age (p = 0.000, p = 0.018, respectively). Analysis of the pathological molecular markers across the four age groups showed that the proportion of patients with larger than 10% area of Ki-67 expression or positive PR expression increased with age (p = 0.000, p = 0.017, respectively). CONCLUSIONS:Appropriate classifications of the age group for risk stratification are 0-14 years old (pediatric group), 15-47 years old (young group), 48-63 years old (middle age group) and ≥ 64 years old (elderly group). This age group classification is effective in evaluating the risk of glioblastoma in glioma patients. 10.1186/s12883-020-01888-w
    Increased rate of positive penicillin skin tests among patients with glioma: insights into the association between allergies and glioma risk. Han Sheng,Huang Yanming,Wang Zixun,Li Zhonghua,Qin Xiaofei,Wu Anhua Journal of neurosurgery OBJECT:Allergy and immunoglobulin E levels are inversely associated with glioma risk. Previous studies have focused on respiratory and food allergies, and little information is available regarding drug allergies. This study evaluated the rate of positive penicillin skin tests (PenSTs) and blood eosinophil counts in a large population of patients with glioma compared with nontumor controls to provide evidence for the relationship between drug allergies and glioma risk. METHODS:A retrospective case-control study was conducted in patients diagnosed with glioma (n = 913) between January 2004 and June 2013. The study patients were matched with nontumor controls (n = 1091) for age, sex, and date of admission to the hospital. Preoperative results of the PenST and eosinophil counts were obtained, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using conditional logistic regression models, while a Kaplan-Meier analysis was used to assess overall survival. RESULTS:The percentage of positive PenSTs was higher among patients with glioma than in control subjects. The age-, sex-, and admission date-adjusted OR for positive versus negative PenSTs was 2.392 (95% CI 1.891-3.026). Eosinophil counts were also higher in glioma cases than in controls: the OR for eosinophil > 0.06 × 10(9)/L versus ≤ 0.06 × 10(9)/L was 1.923 (95% CI 1.608-2.301). There was no association between positive PenST/eosinophil counts and glioma grade or patient survival (n = 105). CONCLUSIONS:In contrast to previously reported relationships between allergy and glioma, in the present study a significantly higher rate of positive PenSTs and higher eosinophil counts were found in patients with glioma than in nontumor controls. These results suggest a complex relationship between allergies and glioma development. 10.3171/2014.7.JNS1412
    Use of tricyclic antidepressants and risk of glioma: a nationwide case-control study. Pottegård Anton,García Rodríguez Luis Alberto,Rasmussen Lotte,Damkier Per,Friis Søren,Gaist David British journal of cancer BACKGROUND:A protective effect of tricyclic antidepressants (TCAs) against gliomas has been suggested by a small number of studies. We investigated this putative association in a nationwide setting. METHODS:Using a case-control design, we identified all patients with histologically verified glioma (cases) in Denmark between 2000 and 2012 and matched these 1 : 20 to population controls. Conditional logistic regression was used to estimate adjusted odds ratios (ORs) for glioma associated with long-term (⩾3 years) use of TCAs. Similar analyses were performed for selective serotonin reuptake inhibitors (SSRIs). RESULTS:We identified 3767 glioma cases and 75 340 population controls. Long-term use of TCAs was inversely associated with risk of glioma (OR 0.72, 95% CI: 0.41-1.25). Long-term SSRI use was not associated with glioma risk (OR 0.93, 95% CI: 0.75-1.16). CONCLUSIONS:Our study indicated that long-term use of TCAs may be associated with a reduced risk of glioma, however, the statistical precision was limited. A similar pattern was not observed for use of SSRIs. 10.1038/bjc.2016.109
    Reproductive factors and risk of glioma in women. Huang Kui,Whelan Elizabeth A,Ruder Avima M,Ward Elizabeth M,Deddens James A,Davis-King Karen E,Carreón Tania,Waters Martha A,Butler Mary Ann,Calvert Geoffrey M,Schulte Paul A,Zivkovich Zachary,Heineman Ellen F,Mandel Jack S,Morton Roscoe F,Reding Douglas J,Rosenman Kenneth D, Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology OBJECTIVE:Glioma is the most common primary malignant brain tumor in adults, responsible for 75% of adult primary malignant brain tumors, yet aside from its association with ionizing radiation, its etiology is poorly understood. Sex differences in brain tumor incidence suggest that hormonal factors may play a role in the etiology of these tumors, but few studies have examined this association in detail. The objective of this study was to explore the role of reproductive factors in the etiology of glioma in women. METHOD:As part of a population-based case-control study, histologically confirmed primary glioma cases (n = 341 women) diagnosed between January 1, 1995 and January 31, 1997 were identified through clinics and hospitals in four Midwest U.S. states. Controls (n = 527 women) were randomly selected from lists of licensed drivers and Health Care Finance Administration enrollees. In-person interviews with subjects (81%) or their proxies (19%) collected reproductive history and other exposure information. RESULTS:Glioma risk increased with older age at menarche (P for trend = 0.009) but only among postmenopausal women. Compared with women who never breast-fed, women who breast-fed >18 months over their lifetime were at increased risk of glioma (odds ratio, 1.8; 95% confidence interval, 1.1-2.9). Women who reported using hormones for symptoms of menopause had a decreased risk of glioma compared with women who never used such hormones (odds ratio, 0.7; 95% confidence interval, 0.5-1.1). CONCLUSION:These results support the hypothesis that reproductive hormones play a role in the etiology of glioma among women.
    Use of Selective Cyclooxygenase-2 Inhibitors, Other Analgesics, and Risk of Glioma. Seliger Corinna,Meier Christoph R,Becker Claudia,Jick Susan S,Bogdahn Ulrich,Hau Peter,Leitzmann Michael F PloS one BACKGROUND:Selective cyclooxygenase-2 (COX-2) inhibitors are analgesic, antipyretic, and anti-inflammatory drugs. They have been found to inhibit the development of glioma in laboratory investigations. Whether these drugs reduce the risk of glioma incidence in humans is unknown. METHODS:We conducted a matched case-control analysis using the U.K.-based Clinical Practice Research Datalink (CPRD). We identified 2,469 cases matched to 24,690 controls on age, sex, calendar time, general practice, and number of years of active history in the CPRD prior to the index date. We conducted conditional logistic regression analyses to determine relative risks, estimated as odds ratios (ORs) with 95% confidence intervals (CIs) of glioma in relation to use of selective COX-2 inhibitors, adjusted for several confounding variables. RESULTS:Use of selective COX-2 inhibitors was unrelated to risk of glioma (adjusted OR for 1-9 versus 0 prescriptions = 1.02; 95% CI = 0.92-1.13, 10-29 versus 0 prescriptions = 1.01; 95% CI = 0.80-1.28, ≥30 versus 0 prescriptions = 1.16; 95% CI = 0.86-1.55). Trends for increasing numbers of prescriptions for other non-steroidal anti-inflammatory drugs (NSAIDs), and non-NSAID analgesics were also not associated with glioma risk. CONCLUSION:Further epidemiologic studies are needed to confirm the null relation of use of selective COX-2 inhibitors to glioma risk and to explain the discrepancy between laboratory investigations and our observational study. IMPACT:Use of selective COX-2 inhibitors is unrelated to glioma risk. 10.1371/journal.pone.0149293
    A case-control study on dietary calcium intake and risk of glioma. Fallah Yekta Masoumeh,Soltani Sanaz,Shayanfar Mehdi,Benisi-Kohansal Sanaz,Mohammad-Shirazi Minoo,Sharifi Giuve,Esmaillzadeh Ahmad European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) Limited evidence exists regarding the association between dietary calcium intake and risk of glioma. The objective of this study was to determine the relationship between dietary calcium intake and risk of glioma in Iranian adults. In this hospital-based case-control study, we enrolled 128 newly-diagnosed cases of glioma and 256 age- and sex-matched controls. Patients with pathologically confirmed glioma (without any other cancers) were selected. Dietary intakes of study participants were collected through a validated 126-item food-frequency questionnaire. Dietary calcium intake was computed from dairy products in the questionnaire. Participants were categorized into quartiles of dietary calcium intake. Binary logistic regression was used to examine the association between dietary calcium intake and glioma. Higher dietary intake of calcium was associated with younger age, long duration of cell phone use, and frequent canned foods intake. After taking age, sex, and energy intake into account, participants with the greatest dietary calcium intake had 84% lower odds of glioma than those with the lowest intake [odds ratio (OR): 0.16; 95% confidence interval (CI), 0.07-0.37]. Further adjustment for other potential confounders including nutrient intakes did not significantly alter the association (OR: 0.22; 95% CI, 0.08-0.64). Even after additional adjustment for BMI, we found a significant inverse association between dietary calcium intake and odds of glioma (OR: 0.23; 95% CI, 0.08-0.65). We found an inverse protective association between high dietary calcium intake and odds of glioma. Further prospective cohort studies are needed to confirm these findings. 10.1097/CEJ.0000000000000629
    Allergy is associated with reduced risk of glioma: A meta-analysis. Zhang C,Zhu Q-X Allergologia et immunopathologia BACKGROUND:Increasing evidences suggest that allergy may reduce the risk of glioma, so it is necessary to perform an up-to-data literature search and investigate this relationship by meta-analysis. METHODS:We identified the included studies by searching PubMed and Web of Science and excluding irrelevant or ineligible articles. Nineteen studies from 15 articles, including 8435 cases and 118,719 controls, were selected for data extraction and synthesis. RESULTS:Pooled outcomes showed that there was an inverse association between allergy and risk of glioma (OR=0.64, 95% CI=0.52-0.78, P<0.001). Meanwhile, asthma and eczema would reduce the risk of glioma by 33% and 23% (OR=0.67, 95% CI=0.59-0.75, P<0.001; OR=0.77, 95% CI=0.68-0.86, P<0.001), respectively. Sensitivity analyses confirmed the stability of these findings. Besides, no publication biases were detected regarding all the investigations. CONCLUSIONS:Overall or specific allergy is protective against glioma. More prospective cohort studies or molecular laboratory experiments are warranted to elucidate the causation and key mechanism. 10.1016/j.aller.2016.12.005
    Occupational solvent exposure and risk of glioma in the INTEROCC study. Benke Geza,Turner Michelle C,Fleming Sarah,Figuerola Jordi,Kincl Laurel,Richardson Lesley,Blettner Maria,Hours Martine,Krewski Daniel,McLean David,Parent Marie-Elise,Sadetzki Siegal,Schlaefer Klaus,Schlehofer Brigitte,Siemiatycki Jack,van Tongeren Martie,Cardis Elisabeth British journal of cancer BACKGROUND:The aetiology of glioma remains largely unknown. Occupational solvent exposure has been suggested as a putative cause of glioma, but past studies have been inconsistent. We examined the association between a range of solvents and glioma risk within the INTEROCC project, a study of brain tumours and occupational exposures based on data from seven national case-control studies conducted in the framework of the INTERPHONE study. We also investigated associations according to tumour grade. METHODS:Data from the seven countries were standardised and then combined into one aggregate data set. Pooled odds ratios (ORs) were estimated for adjusted models that included sex, age, country-region of residence and level of educational attainment. Exposures to any solvent or 11 specific solvents or subgroups were assessed using a modified version of the FINJEM job exposure matrix (JEM) specifically developed for the study, called INTEROCC-JEM. RESULTS:Analysis included 2000 glioma cases and 5565 controls. For glioma and ever/never exposure to any solvent, the OR was 0.91 (95% confidence interval: 0.74-1.11). All ORs were <1.0 for specific solvents/subgroups. There were no increases in risk according to high or low grade of tumour. CONCLUSIONS:The results of this study show no consistent associations for any solvent exposures overall or by grade of tumour. 10.1038/bjc.2017.285
    History of allergies and risk of glioma in adults. Schoemaker Minouk J,Swerdlow Anthony J,Hepworth Sarah J,McKinney Patricia A,van Tongeren Martie,Muir Kenneth R International journal of cancer Epidemiological studies have consistently reported an inverse association between a history of allergic disease and risk of glioma. The reason for this association is unclear, and there is a lack of studies with the detail and size to explore the association in depth. We conducted a UK population-based case-control study with 965 glioma cases and 1,716 controls to investigate glioma risk in relation to allergic disease. Risk was reduced in subjects reporting a history of asthma (odds ratio (OR) = 0.71, 95% confidence interval (CI): 0.54-0.92), hay fever (OR = 0.73, 95% CI: 0.59-0.90), eczema (OR = 0.74, 95% CI: 0.56-0.97) and other allergies (OR = 0.65, 95% CI: 0.47-0.90). Risk was reduced for all the main histological groups. There was no significant trend of risk with age, at the onset of each condition, or the number of conditions reported. Risk reductions were strongest for asthma or hay fever with recent onset. Risk in asthmatic subjects was not related to frequency of use of antiasthmatic drugs, but was significantly reduced for use of antiallergenic medication among subjects with hay fever. The study showed an inverse association of glioma risk with allergic disease. Possible reasons for the association, as well as potential immunological aetiology, include confounding, bias and reverse causality. 10.1002/ijc.22091
    Methylmercury exposure, genetic variation in metabolic enzymes, and the risk of glioma. Creed Jordan H,Peeri Noah C,Anic Gabriella M,Thompson Reid C,Olson Jeffrey J,LaRocca Renato V,Chowdhary Sajeel A,Brockman John D,Gerke Travis A,Nabors Louis B,Egan Kathleen M Scientific reports Methylmercury (MeHg) is an environmental neurotoxin with human exposure mainly from dietary intake of contaminated fish. Exposure to MeHg has been implicated in neurological damage, but research on its role in cancers, specifically glioma, is limited. In a glioma case-control study, we examined associations between toenail mercury (Hg) and glioma risk. We also examined genetic polymorphisms in 13 genes related to MeHg metabolism for association with glioma risk; genetic associations were also studied in the UK Biobank cohort. Median toenail Hg in cases and controls, respectively, was 0.066 μg/g and 0.069 μg/g (interquartile range (IQR): 0.032-0.161 and 0.031-0.150 μg/g). Toenail Hg was not found to be significantly associated with glioma risk (Odds Ratio: 1.02; 95% Confidence Interval: 0.91, 1.14; p = 0.70 in analysis for ordinal trend with increasing quartile of toenail MeHg). No genetic variant was statistically significant in both of the studies; one variant, rs11859163 (MMP2) had a combined p-value of 0.02 though it was no longer significant after adjustment for multiple testing (Bonferroni corrected p = 1). This study does not support the hypothesis that exposure to MeHg plays a role in the development of glioma at levels of exposure found in this study population. 10.1038/s41598-019-47284-4
    Associations of General and Abdominal Obesity with the Risk of Glioma Development. Ahn Stephen,Han Kyungdo,Lee Jung-Eun,Jeun Sin-Soo,Park Yong-Moon,Yang Seung Ho Cancers The association between obesity and the risk of glioma remains unclear. We sought to evaluate the potential association between general and abdominal obesity and the risk of glioma based on a nationwide population-based cohort study of Koreans. Using data from the Korean National Health Insurance System cohort, 6,833,744 people older than 20 years who underwent regular national health examination in both 2009 and 2011 were followed until the end of 2017. We documented 4771 glioma cases based on an ICD-10 code of C71 during the median follow-up period of 7.30 years. Individuals with a body mass index (BMI) ≥ 25.0 kg/m were at significantly higher risk of developing glioma than those with a BMI < 25.0 kg/m (HR 1.08 CI 1.02-1.15). Individuals with a waist circumference (WC) ≥ 90 cm (males)/85 cm (females) also had a significantly higher risk of glioma than those with a WC < 90 cm (males)/85 cm (females) (HR 1.16 CI 1.09-1.24). In the group with a BMI ≥ 25.0 kg/m, individuals with abdominal obesity were at significantly higher risk of developing glioma (HR 1.18 CI 1.09-1.27) than those without abdominal obesity. The role of abdominal obesity in this association was stronger in women than in men. To the best of our knowledge, this is the first demonstration that obese people may be at higher risk of glioma, especially centrally obese people from an Asian population with a BMI ≥ 25.0 kg/m. Loss of visceral fat in people with abdominal obesity may reduce their risk of developing glioma. 10.3390/cancers13122859
    Cigarette smoking and risk of glioma: a prospective cohort study. Silvera Stephanie A Navarro,Miller Anthony B,Rohan Thomas E International journal of cancer The etiology of glioma, the most commonly diagnosed malignant brain tumor among adults in the United States, is poorly understood. N-nitroso compounds are known carcinogens, which are found in cigarette smoke and can induce gliomas in rats. On this basis, it has been hypothesized that cigarette smoking may be associated with an increased risk of glioma. We investigated the association between cigarette smoking and glioma risk in the National Breast Screening Study, which included 89,835 Canadian women aged 40-59 years at recruitment between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths from all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between cigarette smoking and risk of glioma. During a mean of 16.4 years of follow-up, we observed 120 incident glioma cases. Among ever smokers, women who reported having quit smoking had a 51% increase in risk of glioma compared with never smokers (HR = 1.51, 95% CI = 0.97-2.34), while current smokers did not appear to have an increase in risk. When the association with former smokers was further examined by years since quitting, women who had quit smoking >10 years before baseline were at a decreased risk of glioma compared with women who had quit within the 10 years prior to baseline (HR = 0.55, 95% CI = 0.29-1.07), indicating that the association between former smokers and glioma may be driven by women, who recently quit smoking. Compared with nonsmokers, duration of cigarette smoking, number of cigarettes smoked per day and pack-years of smoking were associated with increased glioma risk, although the increases in risk were relatively modest. The present study provides some support for a positive association between cigarette smoking and risk of glioma. 10.1002/ijc.21569
    Mobile phone use and glioma risk: A systematic review and meta-analysis. Yang Ming,Guo WenWen,Yang ChunSheng,Tang JianQin,Huang Qian,Feng ShouXin,Jiang AiJun,Xu XiFeng,Jiang Guan PloS one OBJECTIVE:Many studies have previously investigated the potential association between mobile phone use and the risk of glioma. However, results from these individual studies are inconclusive and controversial. The objective of our study was to investigate the potential association between mobile phone use and subsequent glioma risk using meta-analysis. METHODS:We performed a systematic search of the Science Citation Index Embase and PubMed databases for studies reporting relevant data on mobile phone use and glioma in 1980-2016. The data were extracted and measured in terms of the odds ratio (OR) and 95% confidence interval (CI) using the random effects model. Subgroup analyses were also carried out. This meta-analysis eventually included 11 studies comprising a total 6028 cases and 11488 controls. RESULTS:There was a significant positive association between long-term mobile phone use (minimum, 10 years) and glioma (OR = 1.44, 95% CI = 1.08-1.91). And there was a significant positive association between long-term ipsilateral mobile phone use and the risk of glioma (OR = 1.46, 95% CI = 1.12-1.92). Long-term mobile phone use was associated with 2.22 times greater odds of low-grade glioma occurrence (OR = 2.22, 95% CI = 1.69-2.92). Mobile phone use of any duration was not associated with the odds of high-grade glioma (OR = 0.81, 95% CI = 0.72-0.92). Contralateral mobile phone use was not associated with glioma regardless of the duration of use. Similarly, this association was not observed when the analysis was limited to high-grade glioma. CONCLUSIONS:Our results suggest that long-term mobile phone use may be associated with an increased risk of glioma. There was also an association between mobile phone use and low-grade glioma in the regular use or long-term use subgroups. However, current evidence is of poor quality and limited quantity. It is therefore necessary to conduct large sample, high quality research or better characterization of any potential association between long-term ipsilateral mobile phone use and glioma risk. 10.1371/journal.pone.0175136
    Known glioma risk loci are associated with glioma with a family history of brain tumours -- a case-control gene association study. Melin Beatrice,Dahlin Anna M,Andersson Ulrika,Wang Zhaoming,Henriksson Roger,Hallmans Göran,Bondy Melissa L,Johansen Christoffer,Feychting Maria,Ahlbom Anders,Kitahara Cari M,Wang Sophia S,Ruder Avima M,Carreón Tania,Butler Mary Ann,Inskip Peter D,Purdue Mark,Hsing Ann W,Mechanic Leah,Gillanders Elizabeth,Yeager Meredith,Linet Martha,Chanock Stephen J,Hartge Patricia,Rajaraman Preetha International journal of cancer Familial cancer can be used to leverage genetic association studies. Recent genome-wide association studies have reported independent associations between seven single nucleotide polymorphisms (SNPs) and risk of glioma. The aim of this study was to investigate whether glioma cases with a positive family history of brain tumours, defined as having at least one first- or second-degree relative with a history of brain tumour, are associated with known glioma risk loci. One thousand four hundred and thirty-one glioma cases and 2,868 cancer-free controls were identified from four case-control studies and two prospective cohorts from USA, Sweden and Denmark and genotyped for seven SNPs previously reported to be associated with glioma risk in case-control designed studies. Odds ratios were calculated by unconditional logistic regression. In analyses including glioma cases with a family history of brain tumours (n = 104) and control subjects free of glioma at baseline, three of seven SNPs were associated with glioma risk: rs2736100 (5p15.33, TERT), rs4977756 (9p21.3, CDKN2A-CDKN2B) and rs6010620 (20q13.33, RTEL1). After Bonferroni correction for multiple comparisons, only one marker was statistically significantly associated with glioma risk, rs6010620 (ORtrend for the minor (A) allele, 0.39; 95% CI: 0.25-0.61; Bonferroni adjusted ptrend , 1.7 × 10(-4) ). In conclusion, as previously shown for glioma regardless of family history of brain tumours, rs6010620 (RTEL1) was associated with an increased risk of glioma when restricting to cases with family history of brain tumours. These findings require confirmation in further studies with a larger number of glioma cases with a family history of brain tumours. 10.1002/ijc.27922
    Meta-analysis of association between mobile phone use and glioma risk. Wang Yabo,Guo Xiaqing Journal of cancer research and therapeutics OBJECTIVE:The purpose of this study was to evaluate the association between mobile phone use and glioma risk through pooling the published data. METHODS:By searching Medline, EMBSE, and CNKI databases, we screened the open published case-control or cohort studies about mobile phone use and glioma risk by systematic searching strategy. The pooled odds of mobile use in glioma patients versus healthy controls were calculated by meta-analysis method. The statistical analysis was done by Stata12.0 software (http://www.stata.com). RESULTS:After searching the Medline, EMBSE, and CNKI databases, we ultimately included 11 studies range from 2001 to 2008. For ≥1 year group, the data were pooled by random effects model. The combined data showed that there was no association between mobile phone use and glioma odds ratio (OR) =1.08 (95% confidence interval [CI]: 0.91-1.25,P > 0.05). However, a significant association was found between mobile phone use more than 5 years and glioma risk OR = 1.35 (95% CI: 1.09-1.62, P < 0.05). The publication bias of this study was evaluated by funnel plot and line regression test. The funnel plot and line regression test (t = 0.25,P = 0.81) did not indicate any publication bias. CONCLUSION:Long-term mobile phone use may increase the risk of developing glioma according to this meta-analysis. 10.4103/0973-1482.200759
    Approaching a Scientific Consensus on the Association between Allergies and Glioma Risk: A Report from the Glioma International Case-Control Study. Amirian E Susan,Zhou Renke,Wrensch Margaret R,Olson Sara H,Scheurer Michael E,Il'yasova Dora,Lachance Daniel,Armstrong Georgina N,McCoy Lucie S,Lau Ching C,Claus Elizabeth B,Barnholtz-Sloan Jill S,Schildkraut Joellen,Ali-Osman Francis,Sadetzki Siegal,Johansen Christoffer,Houlston Richard S,Jenkins Robert B,Bernstein Jonine L,Merrell Ryan T,Davis Faith G,Lai Rose,Shete Sanjay,Amos Christopher I,Melin Beatrice S,Bondy Melissa L Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology BACKGROUND:Several previous studies have found inverse associations between glioma susceptibility and a history of allergies or other atopic conditions. Some evidence indicates that respiratory allergies are likely to be particularly relevant with regard to glioma risk. Using data from the Glioma International Case-Control Study (GICC), we examined the effects of respiratory allergies and other atopic conditions on glioma risk. METHODS:The GICC contains detailed information on history of atopic conditions for 4,533 cases and 4,171 controls, recruited from 14 study sites across five countries. Using two-stage random-effects restricted maximum likelihood modeling to calculate meta-analysis ORs, we examined the associations between glioma and allergy status, respiratory allergy status, asthma, and eczema. RESULTS:Having a history of respiratory allergies was associated with an approximately 30% lower glioma risk, compared with not having respiratory allergies (mOR, 0.72; 95% confidence interval, 0.58-0.90). This association was similar when restricting to high-grade glioma cases. Asthma and eczema were also significantly protective against glioma. CONCLUSION:A substantial amount of data on the inverse association between atopic conditions and glioma has accumulated, and findings from the GICC study further strengthen the existing evidence that the relationship between atopy and glioma is unlikely to be coincidental. IMPACT:As the literature approaches a consensus on the impact of allergies in glioma risk, future research can begin to shift focus to what the underlying biologic mechanism behind this association may be, which could, in turn, yield new opportunities for immunotherapy or cancer prevention. 10.1158/1055-9965.EPI-15-0847
    Statin use and risk of glioma: population-based case-control analysis. Seliger Corinna,Meier Christoph Rudolf,Becker Claudia,Jick Susan Sara,Bogdahn Ulrich,Hau Peter,Leitzmann Michael Fred European journal of epidemiology Statins have been reported to decrease the incidence of cancer, but the risk of glioma among statin users has been investigated in only two prior observational studies, both of them suggesting a modest protective effect of statins. We conducted a matched case-control study using data from the UK-based Clinical Practice Research Datalink to analyse use of statins among 2469 cases with glioma and 24,690 controls. We performed conditional logistic regression analysis to calculate relative risks, estimated as odds ratios (ORs) with 95 % confidence intervals (CIs) adjusting for multiple confounding factors. As compared with non-use of statins, use of statins was not associated with risk of glioma (OR for ≥90 prescriptions=0.75; 95 % CI 0.48-1.17). Our findings do not support previous sparse evidence of a possible inverse association between statin use and glioma risk. 10.1007/s10654-016-0145-7
    Circadian pathway genes in relation to glioma risk and outcome. Madden Melissa H,Anic Gabriella M,Thompson Reid C,Nabors L Burton,Olson Jeffrey J,Browning James E,Monteiro Alvaro N,Egan Kathleen M Cancer causes & control : CCC PURPOSE:There is growing evidence that circadian disruption may alter risk and aggressiveness of cancer. We evaluated common genetic variants in the circadian gene pathway for associations with glioma risk and patient outcome in a US clinic-based case-control study. METHODS:Subjects were genotyped for 17 candidate single nucleotide polymorphisms in ARNTL, CRY1, CRY2, CSNK1E, KLHL30, NPAS2, PER1, PER3, CLOCK, and MYRIP. Unconditional logistic regression was used to estimate age and gender-adjusted odds ratios (OR) and 95 % confidence intervals (CI) for glioma risk under three inheritance models (additive, dominant, and recessive). Proportional hazards regression was used to estimate hazard ratios for glioma-related death among 441 patients with high-grade tumors. Survival associations were validated using The Cancer Genome Atlas (TCGA) dataset. RESULTS:A variant in PER1 (rs2289591) was significantly associated with overall glioma risk (per variant allele OR 0.80; 95 % CI 0.66-0.97; p trend = 0.027). The variant allele for CLOCK rs11133391 under a recessive model increased risk of oligodendroglioma (OR 2.41; 95 % CI 1.31-4.42; p = 0.005), though not other glioma subtypes (p for heterogeneity = 0.0033). The association remained significant after false discovery rate adjustment (p = 0.008). Differential associations by gender were observed for MYRIP rs6599077 and CSNK1E rs1534891 though differences were not significant after adjustment for multiple testing. No consistent mortality associations were identified. Several of the examined genes exhibited differential expression in glioblastoma multiforme versus normal brain in TCGA data (MYRIP, ARNTL, CRY1, KLHL30, PER1, CLOCK, and PER3), and expression of NPAS2 was significantly associated with a poor patient outcome in TCGA patients. CONCLUSION:This exploratory analysis provides some evidence supporting a role for circadian genes in the onset of glioma and possibly the outcome of glioma. 10.1007/s10552-013-0305-y
    Smoking and risk of glioma: a meta-analysis. Mandelzweig Lori,Novikov Ilya,Sadetzki Siegal Cancer causes & control : CCC OBJECTIVE:Although causal relationships between smoking and cancer risk have been established for many sites, most studies of brain cancer have not supported an association. However, two recent cohort studies showed increased risks of glioma among smokers. We quantified the association between smoking and glioma through a meta-analysis of the literature. METHODS:Of 20 eligible studies, 17 (6 cohort and 11 case–control) were included in an analysis of ever versus never smoking. Multivariate-adjusted risk estimates in the papers were pooled to calculate cumulative risk. RESULTS:The cumulative estimated risk associated with ever smoking was 1.06 (95% CI: 0.97–1.15), for all, 1.10 (95% CI: 1.01–1.20) for cohort, and 1.00 (95% CI: 0.88–1.15) for case–control studies. A significantly increased risk associated with past smoking was noted for cohort studies, OR = 1.16 (p = 0.007), while an increased risk of borderline significance was seen for all studies, OR = 1.10 (p = 0.08). In general, dose–response analysis did not support an association and was limited because very few studies included these variables and could be pooled. CONCLUSION:Overall, results of pooling of all studies suggested that smoking is not associated with risk of glioma. However, the small but significant increased risk seen for cohort studies remains to be clarified. 10.1007/s10552-009-9386-z
    Association between adult height, genetic susceptibility and risk of glioma. Kitahara Cari M,Wang Sophia S,Melin Beatrice S,Wang Zhaoming,Braganza Melissa,Inskip Peter D,Albanes Demetrius,Andersson Ulrika,Beane Freeman Laura E,Buring Julie E,Carreón Tania,Feychting Maria,Gapstur Susan M,Gaziano J Michael,Giles Graham G,Hallmans Goran,Hankinson Susan E,Henriksson Roger,Hsing Ann W,Johansen Christoffer,Linet Martha S,McKean-Cowdin Roberta,Michaud Dominique S,Peters Ulrike,Purdue Mark P,Rothman Nathaniel,Ruder Avima M,Sesso Howard D,Severi Gianluca,Shu Xiao-Ou,Stevens Victoria L,Visvanathan Kala,Waters Martha A,White Emily,Wolk Alicja,Zeleniuch-Jacquotte Anne,Zheng Wei,Hoover Robert,Fraumeni Joseph F,Chatterjee Nilanjan,Yeager Meredith,Chanock Stephen J,Hartge Patricia,Rajaraman Preetha International journal of epidemiology BACKGROUND:Some, but not all, observational studies have suggested that taller stature is associated with a significant increased risk of glioma. In a pooled analysis of observational studies, we investigated the strength and consistency of this association, overall and for major sub-types, and investigated effect modification by genetic susceptibility to the disease. METHODS:We standardized and combined individual-level data on 1354 cases and 4734 control subjects from 13 prospective and 2 case-control studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for glioma and glioma sub-types were estimated using logistic regression models stratified by sex and adjusted for birth cohort and study. Pooled ORs were additionally estimated after stratifying the models according to seven recently identified glioma-related genetic variants. RESULTS:Among men, we found a positive association between height and glioma risk (≥ 190 vs 170-174 cm, pooled OR = 1.70, 95% CI: 1.11-2.61; P-trend = 0.01), which was slightly stronger after restricting to cases with glioblastoma (pooled OR = 1.99, 95% CI: 1.17-3.38; P-trend = 0.02). Among women, these associations were less clear (≥ 175 vs 160-164 cm, pooled OR for glioma = 1.06, 95% CI: 0.70-1.62; P-trend = 0.22; pooled OR for glioblastoma = 1.36, 95% CI: 0.77-2.39; P-trend = 0.04). In general, we did not observe evidence of effect modification by glioma-related genotypes on the association between height and glioma risk. CONCLUSION:An association of taller adult stature with glioma, particularly for men and stronger for glioblastoma, should be investigated further to clarify the role of environmental and genetic determinants of height in the etiology of this disease. 10.1093/ije/dys114
    Association between fish intake and glioma risk: a systematic review and meta-analysis. Lei Honcho,To Chiho,Lei Unpeng The Journal of international medical research OBJECTIVES:We investigated the association between the consumption of fresh and processed fish and glioma risk using a meta-analysis approach. METHODS:We selected and analyzed observational studies that discussed the relationships between fresh and processed fish intake on glioma risk from PubMed, Web of Science, Embase, and the SinoMed and Wanfang databases from inception to 31 March 2020. Studies were selected according to pre-established eligibility criteria and data were extracted separately by two researchers. A meta-analysis was conducted based on a random-effects model to provide pooled odds ratios (OR) and 95% confidence intervals (CIs). RESULTS:Eight studies considered the relationship between fish intake (seven fresh and seven processed fish) and glioma risk and were included in this meta-analysis. The OR effect size for fresh fish intake and glioma risk was 0.72 (95%CI 0.53-0.97) and the overall OR effect size for processed fish intake and glioma risk was 1.88 (95%CI 1.06-3.34). CONCLUSION:Dietary intake of fresh fish may reduce the risk of glioma, but consumption of processed fish may increase the risk of glioma. This study had some limitations, and further studies are therefore required to clarify the associations between fish intake and glioma risk. 10.1177/0300060520939695
    Allergy and glioma risk: test of association by genotype. Dobbins Sara E,Hosking Fay J,Shete Sanjay,Armstrong Georgina,Swerdlow Anthony,Liu Yanhong,Yu Robert,Lau Ching,Schoemaker Minouk J,Hepworth Sarah J,Muir Kenneth,Bondy Melissa,Houlston Richard S International journal of cancer Although epidemiological studies have suggested an association between atopy and glioma risk, these observations have been based on self-reporting of allergic conditions raising the possibility that associations may be noncausal and arise as a consequence of bias, reverse causation or other artifacts. Genetic information provides an alternative approach to investigate the relationship avoiding such biases. We analyzed 1,878 glioma cases and 3,670 controls for variants at 2q12, 5q12.1, 11q13 and 17q21 that are associated with asthma or eczema risk at p < 5.0 × 10(-7) . The SNP rs7216389, which tags the 3' flanking region of ORMDL3 at 17q21 and has been associated with childhood asthma, was correlated with increased glioma risk (OR = 1.10; 95% CI: 1.01-1.19). These data provide evidence for a correlation between asthma susceptibility and glioma risk and illustrate the value of using genetics as an investigative tool for developing etiological hypotheses. 10.1002/ijc.25483
    Diabetes, use of antidiabetic drugs, and the risk of glioma. Seliger Corinna,Ricci Cristian,Meier Christoph R,Bodmer Michael,Jick Susan S,Bogdahn Ulrich,Hau Peter,Leitzmann Michael F Neuro-oncology BACKGROUND:Prior epidemiologic studies suggest inverse relations between diabetes and glioma risk, but the underlying mechanisms, including use of antidiabetic drugs, are unknown. METHODS:We therefore performed a matched case-control analysis using the Clinical Practice Research Datalink (CPRD). We identified incident glioma cases diagnosed between 1995 and 2012 and matched each case with 10 controls on age, gender, calendar time, general practice, and years of active history in the CPRD. We performed conditional logistic regression to estimate odds ratios (ORs) with 95% CIs, adjusted for body mass index and smoking. RESULTS:We identified 2005 cases and 20 050 controls. Diabetes was associated with decreased risk of glioma (OR = 0.74; 95% CI = 0.60-0.93), particularly glioblastoma (OR = 0.69; 95% CI = 0.51-0.94). Glioblastoma risk reduction was markedly pronounced among diabetic men (OR = 0.60; 95% CI = 0.40-0.90), most apparently for those with diabetes of long-term duration (OR for >5 vs 0 y = 0.46; 95% CI = 0.26-0.82) or poor glycemic control (OR for HbA1c ≥ 8 vs <6.5% = 0.20; 95% CI = 0.06-0.70). In contrast, the effect of diabetes on glioblastoma risk was absent among women (OR = 0.85; 95% CI = 0.53-1.36). No significant associations with glioma were found for use of metformin (OR for ≥ 30 vs 0 prescriptions = 0.72; 95% CI = 0.38-1.39), sulfonylureas (OR = 0.71; 95% CI = 0.39-1.30), or insulin (OR = 0.79; 95% CI = 0.37-1.69). CONCLUSIONS:Antidiabetic treatment appears to be unrelated to glioma, but long-term diabetes duration and increased HbA1c both show decreased glioma risk. Stronger findings in men than women suggest low androgen levels concurrent with diabetes as a biologic mechanism. 10.1093/neuonc/nov100
    Asthma and risk of glioma: a population-based case-control study. Kaur Harsheen,Lachance Daniel H,Ryan Conor S,Sheen Youn Ho,Seol Hee Yun,Wi Chung-Il,Sohn Sunghwan,King Katherine S,Ryu Euijung,Juhn Young BMJ open OBJECTIVES:Literature suggests an inconsistent, but largely inverse, association between asthma and risk of glioma, which is primarily due to methodological inconsistency in sampling frame and ascertainment of asthma. The objective of the study was to clarify the association between asthma and risk of glioma by minimising methodological biases (eg, recall and detection bias). DESIGN:A population-based case-control study. SETTING:General population in Olmsted County, Minnesota, USA. PARTICIPANTS:All eligible biopsy-proven incident glioma cases (1995-2014) and two sets of controls among residents matched to age and sex (first set: community controls without glioma; second set: MRI-negative controls from the same community). METHODS:The predetermined asthma criteria via medical record review were applied to ascertain asthma status of cases and controls. History of asthma prior to index date was compared between glioma cases and their matched controls using conditional logistic regression models. Propensity score for asthma status was adjusted for multivariate analysis. RESULTS:We enrolled 135 glioma cases (median age at index date: 53 years) and 270 controls. Of the cases, 21 had a history of asthma (16%), compared with 36 of MRI controls (27%) (OR (95% CI) 0.48 (0.26 to 0.91), p=0.03). With MRI controls, an inverse association between asthma and risk of glioma persisted after adjusting for the propensity score for asthma status, but did not reach statistical significance probably due to the lack of statistical power (OR (95% CI) 0.48 (0.21 to 1.09); p=0.08). Based on comparison of characteristics of controls and cases, community controls seem to be more susceptible to a detection bias. CONCLUSIONS:While differential detection might account for the association between asthma and risk of glioma, asthma may potentially pose a protective effect on risk of glioma. Our study results need to be replicated by a larger study. 10.1136/bmjopen-2018-025746
    Autoimmune diseases and immunosuppressive therapy in relation to the risk of glioma. Anssar Tareq M,Leitzmann Michael F,Linker Ralf A,Meier Christoph,Becker Claudia,Jick Susan,Sahm Katharina,Platten Michael,Hau Peter,Seliger Corinna Cancer medicine Effectors from the immune system can modulate the course and possibly the early development of gliomas. We, therefore, hypothesized that autoimmune diseases associated with increased immune-surveillance may also modulate the risk of human glioma. To test this hypothesis, we used data from the well-validated Clinical Practice Research Datalink (CPRD) GOLD from the UK to analyze the association of immune-related disorders or use of immunosuppressive drugs and the risk of glioma. We identified 3112 incident glioma cases diagnosed between 1995 and 2017. We randomly selected up to 10 controls, matching them to glioma cases on age, sex, index date, general practice, and number of years of active history in the database prior to the index date. We performed conditional logistic regression analyses to estimate Odds Ratios (ORs) of glioma among those exposed to allergies, autoimmune diseases, and immunosuppressive drugs. Overall, we found no materially altered association between a history of any autoimmune disease (OR 0.98, 95% CI 0.86-1.11), allergy (OR 0.97, 95% CI 0.89-1.05), or use of immunosuppressive drugs and the risk of glioma. However, subgroup analyses among younger patients found a statistically significant increased risk of glioma in patients with a history of inflammatory bowel disease (IBD) (OR 2.59, 95% CI 1.31-5.12). There was also an inverse association between asthma and risk of glioma in patients with longer survival (OR 0.73, 95% CI 0.58-0.91) and between long-term duration diabetes and risk of glioma (OR 0.71, 95% CI 0.53-0.96). 10.1002/cam4.2767
    Adiposity at different periods of life and risk of adult glioma in a cohort of postmenopausal women. Kabat Geoffrey C,Rohan Thomas E Cancer epidemiology BACKGROUND:Little is known about risk factors for adult glioma. Adiposity has received some attention as a possible risk factor. METHODS:We examined the association of body mass index (BMI), waist circumference (WC) and waist-to-hip ratio (WHR), measured at enrollment, as well as self-reported weight earlier in life, with risk of glioma in a large cohort of postmenopausal women. Over 18 years of follow-up, 217 glioma cases were ascertained, including 164 glioblastomas. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals. RESULTS:There was a modest, non-significant trend toward increasing risk of glioma and glioblastoma with increasing measured BMI and WHR. No trend was seen for WC. Self-reported BMI earlier in life showed no association with risk. CONCLUSIONS:Our weak findings regarding the association of adiposity measures with risk of glioma are in agreement the results of several large cohort studies. In view of the available evidence, adiposity is unlikely to represent an important risk factor for glioma. 10.1016/j.canep.2018.03.008
    A prospective study of tea and coffee intake and risk of glioma. Cote David J,Bever Alaina M,Wilson Kathryn M,Smith Timothy R,Smith-Warner Stephanie A,Stampfer Meir J International journal of cancer Tea and coffee have antioxidant and neuroprotective effects. Observational studies suggest that tea and coffee intake may reduce cancer risk, but data on glioma risk are inconclusive. We evaluated the association between tea, coffee and caffeine intake and glioma risk in the female Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII) and the male Health Professionals Follow-Up Study (HPFS). Cumulative intake was derived from validated quadrennial food frequency questionnaires. Glioma cases were confirmed by medical record review. Multivariable-adjusted hazard ratios of glioma by beverage intake category were estimated using Cox proportional hazards models. We documented 554 incident cases of glioma (256 in NHS, 87 in NHSII and 211 in HPFS). Compared to <1 cup/week, higher tea consumption was borderline inversely associated with glioma risk in pooled cohorts (hazard ratio [HR] = 0.73, 95% confidence interval [CI]: 0.49-1.10 for >2 cups/day, p-trend = 0.05), but not in women (HR = 0.74, 95% CI: 0.47-1.18 for >2 cups/day, p-trend = 0.11) or men (HR = 0.70, 95% CI: 0.30-1.60 for >2 cups/day, p-trend = 0.30) separately. Overall, we observed no significant associations between caffeinated, decaffeinated or total coffee intake and glioma risk. There were no material differences in the results with baseline values, 8-year lagged responses, or when limited to glioblastoma (n = 362). In three large prospective cohort studies, tea intake was borderline inversely associated with glioma risk. No significant associations were observed for coffee intake and glioma risk. These results merit further exploration in prospective studies. 10.1002/ijc.32574
    Testing for causality between systematically identified risk factors and glioma: a Mendelian randomization study. Howell A E,Robinson J W,Wootton R E,McAleenan A,Tsavachidis S,Ostrom Q T,Bondy M,Armstrong G,Relton C,Haycock P,Martin R M,Zheng J,Kurian K M BMC cancer BACKGROUND:Whilst epidemiological studies have provided evidence of associations between certain risk factors and glioma onset, inferring causality has proven challenging. Using Mendelian randomization (MR), we assessed whether associations of 36 reported glioma risk factors showed evidence of a causal relationship. METHODS:We performed a systematic search of MEDLINE from inception to October 2018 to identify candidate risk factors and conducted a meta-analysis of two glioma genome-wide association studies (5739 cases and 5501 controls) to form our exposure and outcome datasets. MR analyses were performed using genetic variants to proxy for candidate risk factors. We investigated whether risk factors differed by subtype diagnosis (either glioblastoma (n = 3112) or non-glioblastoma (n = 2411)). MR estimates for each risk factor were determined using multiplicative random effects inverse-variance weighting (IVW). Sensitivity analyses investigated potential pleiotropy using MR-Egger regression, the weighted median estimator, and the mode-based estimator. To increase power, trait-specific polygenic risk scores were used to test the association of a genetically predicated increase in each risk factor with glioma onset. RESULTS:Our systematic search identified 36 risk factors that could be proxied using genetic variants. Using MR, we found evidence that four genetically predicted traits increased risk of glioma, glioblastoma or non-glioblastoma: longer leukocyte telomere length, liability to allergic disease, increased alcohol consumption and liability to childhood extreme obesity (> 3 standard deviations from the mean). Two traits decreased risk of non-glioblastoma cancers: increased low-density lipoprotein cholesterol (LDLc) and triglyceride levels. Our findings were similar across sensitivity analyses that made allowance for pleiotropy (genetic confounding). CONCLUSIONS:Our comprehensive investigation provides evidence of a causal link between both genetically predicted leukocyte telomere length, allergic disease, alcohol consumption, childhood extreme obesity, and LDLc and triglyceride levels, and glioma. The findings from our study warrant further research to uncover mechanisms that implicate these traits in glioma onset. 10.1186/s12885-020-06967-2
    Joint effects between five identified risk variants, allergy, and autoimmune conditions on glioma risk. Safaeian Mahboobeh,Rajaraman Preetha,Hartge Patricia,Yeager Meredith,Linet Martha,Butler Mary Ann,Ruder Avima M,Purdue Mark P,Hsing Ann,Beane-Freeman Laura,Hoppin Jane A,Albanes Demetrius,Weinstein Stephanie J,Inskip Peter D,Brenner Alina,Rothman Nathaniel,Chatterjee Nilanjan,Gillanders Elizabeth M,Chanock Stephen J,Wang Sophia S Cancer causes & control : CCC Common variants in two of the five genetic regions recently identified from genome-wide association studies (GWAS) of risk of glioma were reported to interact with a history of allergic symptoms. In a pooled analysis of five epidemiologic studies, we evaluated the association between the five GWAS implicated gene variants and allergies and autoimmune conditions (AIC) on glioma risk (851 adult glioma cases and 3,977 controls). We further evaluated the joint effects between allergies and AIC and these gene variants on glioma risk. Risk estimates were calculated as odds ratios (OR) and 95 % confidence intervals (95 % CI), adjusted for age, gender, and study. Joint effects were evaluated by conducting stratified analyses whereby the risk associations (OR and 95 % CI) with the allergy or autoimmune conditions for glioma were evaluated by the presence or absence of the 'at-risk' variant, and estimated p interaction by fitting models with the main effects of allergy or autoimmune conditions and genotype and an interaction (product) term between them. Four of the five SNPs previously reported by others were statistically significantly associated with increased risk of glioma in our study (rs2736100, rs4295627, rs4977756, and rs6010620); rs498872 was not associated with glioma in our study. Reporting any allergies or AIC was associated with reduced risks of glioma (allergy: adjusted OR = 0.71, 95 % CI 0.55-0.91; AIC: adjusted OR = 0.65, 95 % CI 0.47-0.90). We did not observe differential association between allergic or autoimmune conditions and glioma by genotype, and there were no statistically significant p interactions. Stratified analysis by glioma grade (low and high grade) did not suggest risk differences by disease grade. Our results do not provide evidence that allergies or AIC modulate the association between the four GWAS-identified SNPs examined and risk of glioma. 10.1007/s10552-013-0244-7
    Allergy and risk of glioma: a meta-analysis. Chen C,Xu T,Chen J,Zhou J,Yan Y,Lu Y,Wu S European journal of neurology We evaluated the association between allergic conditions and the risk of glioma in case-control and cohort studies published so far on this issue. A total of 12 studies (10 case-control and 2 cohort studies) were included in the analysis, involving 61 090 participants, of whom 6408 had glioma. When compared with non-allergic conditions, the pooled odds ratio (OR) with any allergic conditions for glioma was 0.60 (95% CI: 0.52-0.69, P<0.001), suggesting a significant negative association (protective effect) between allergy and glioma. Subgroup analysis showed that the ORs were 0.70 (95% CI: 0.62-0.79, P<0.001), 0.69 (95% CI: 0.62-0.78, P<0.001), and 0.78 (95% CI: 0.70-0.87, P<0.001) for asthma, eczema, and hay fever, respectively. The significant association remained even after excluding the bias of proxy reporting (OR=0.61; 95% CI: 0.50-0.75, P<0.001). We conclude that allergic conditions may significantly reduce the risk of glioma. 10.1111/j.1468-1331.2010.03187.x
    History of chickenpox in glioma risk: a report from the glioma international case-control study (GICC). Amirian E Susan,Scheurer Michael E,Zhou Renke,Wrensch Margaret R,Armstrong Georgina N,Lachance Daniel,Olson Sara H,Lau Ching C,Claus Elizabeth B,Barnholtz-Sloan Jill S,Il'yasova Dora,Schildkraut Joellen,Ali-Osman Francis,Sadetzki Siegal,Jenkins Robert B,Bernstein Jonine L,Merrell Ryan T,Davis Faith G,Lai Rose,Shete Sanjay,Amos Christopher I,Melin Beatrice S,Bondy Melissa L Cancer medicine Varicella zoster virus (VZV) is a neurotropic α-herpesvirus that causes chickenpox and establishes life-long latency in the cranial nerve and dorsal root ganglia of the host. To date, VZV is the only virus consistently reported to have an inverse association with glioma. The Glioma International Case-Control Study (GICC) is a large, multisite consortium with data on 4533 cases and 4171 controls collected across five countries. Here, we utilized the GICC data to confirm the previously reported associations between history of chickenpox and glioma risk in one of the largest studies to date on this topic. Using two-stage random-effects restricted maximum likelihood modeling, we found that a positive history of chickenpox was associated with a 21% lower glioma risk, adjusting for age and sex (95% confidence intervals (CI): 0.65-0.96). Furthermore, the protective effect of chickenpox was stronger for high-grade gliomas. Our study provides additional evidence that the observed protective effect of chickenpox against glioma is unlikely to be coincidental. Future studies, including meta-analyses of the literature and investigations of the potential biological mechanism, are warranted. 10.1002/cam4.682
    Reproductive factors and risk of meningioma and glioma. Wigertz Annette,Lönn Stefan,Hall Per,Auvinen Anssi,Christensen Helle Collatz,Johansen Christoffer,Klaeboe Lars,Salminen Tiina,Schoemaker Minouk J,Swerdlow Anthony J,Tynes Tore,Feychting Maria Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology Female sex hormones have previously been suggested as possible risk factors for brain tumors, but published studies have reported conflicting results. We conducted a population-based case-control study of glioma (n=626) and meningioma (n=906) cases and randomly selected controls stratified on age and geographic region (n=1,774) in Denmark, Finland, Norway, Sweden, and the United Kingdom. Unconditional logistic regression was used to estimate odds ratios (OR) for glioma and meningioma in relation to reproductive factors. A decreased glioma risk was associated with ever-pregnancy compared with never-pregnancy [OR, 0.8; 95% confidence interval (95% CI), 0.6-1.0]. Meningioma risk among women ages <50 years was increased in relation to number of pregnancies leading to a live birth (OR, 1.8; 95% CI: 1.1-2.8 for giving birth to 3 children compared with nulliparous women; P(trend) among parous women=0.01). This relation was not found for older women. Breast-feeding among parous women increased the glioma risk (OR, 2.2; 95% CI, 1.3-3.9 for breast-feeding 36 months or more compared with breast-feeding 3 months or less). Menopausal status and age at menopause were not associated with meningioma or glioma risk. Our findings imply that reproductive hormones may influence the occurrence of meningioma and glioma. 10.1158/1055-9965.EPI-08-0406
    Understanding inherited genetic risk of adult glioma - a review. Rice Terri,Lachance Daniel H,Molinaro Annette M,Eckel-Passow Jeanette E,Walsh Kyle M,Barnholtz-Sloan Jill,Ostrom Quinn T,Francis Stephen S,Wiemels Joseph,Jenkins Robert B,Wiencke John K,Wrensch Margaret R Neuro-oncology practice During the past six years, researchers have made major progress identifying common inherited genetic variation that increases risk for primary adult glioma. This paper summarizes knowledge about rare familial cancer syndromes that include adult glioma and reviews the available literature on the more recently discovered common inherited variation. Ten independent inherited variants in eight chromosomal regions have been convincingly associated with increased risk for adult glioma. Most of these variants increase relative risk of primary adult glioma by 20% to 40%, but the TP53 variant rs78378222 confers a two-fold relative risk (ie, 200%), and rs557505857 on chromosome 8 confers a six-fold relative risk of -mutated astrocytomas and oligodendroglial tumors (ie, 600%). Even with a six-fold relative risk, the overall risk of developing adult glioma is too low for screening for the high-risk variant on chromosome 8. Future studies will help clarify which inherited adult glioma risk variants are associated with subtypes defined by histology and/or acquired tumor mutations. This review also provides an information sheet for primary adult glioma patients and their families. 10.1093/nop/npv026
    Influence of obesity-related risk factors in the aetiology of glioma. Disney-Hogg Linden,Sud Amit,Law Philip J,Cornish Alex J,Kinnersley Ben,Ostrom Quinn T,Labreche Karim,Eckel-Passow Jeanette E,Armstrong Georgina N,Claus Elizabeth B,Il'yasova Dora,Schildkraut Joellen,Barnholtz-Sloan Jill S,Olson Sara H,Bernstein Jonine L,Lai Rose K,Swerdlow Anthony J,Simon Matthias,Hoffmann Per,Nöthen Markus M,Jöckel Karl-Heinz,Chanock Stephen,Rajaraman Preetha,Johansen Christoffer,Jenkins Robert B,Melin Beatrice S,Wrensch Margaret R,Sanson Marc,Bondy Melissa L,Houlston Richard S British journal of cancer BACKGROUND:Obesity and related factors have been implicated as possible aetiological factors for the development of glioma in epidemiological observation studies. We used genetic markers in a Mendelian randomisation framework to examine whether obesity-related traits influence glioma risk. This methodology reduces bias from confounding and is not affected by reverse causation. METHODS:Genetic instruments were identified for 10 key obesity-related risk factors, and their association with glioma risk was evaluated using data from a genome-wide association study of 12,488 glioma patients and 18,169 controls. The estimated odds ratio of glioma associated with each of the genetically defined obesity-related traits was used to infer evidence for a causal relationship. RESULTS:No convincing association with glioma risk was seen for genetic instruments for body mass index, waist-to-hip ratio, lipids, type-2 diabetes, hyperglycaemia or insulin resistance. Similarly, we found no evidence to support a relationship between obesity-related traits with subtypes of glioma-glioblastoma (GBM) or non-GBM tumours. CONCLUSIONS:This study provides no evidence to implicate obesity-related factors as causes of glioma. 10.1038/s41416-018-0009-x
    Aspirin, NSAIDs, and Glioma Risk: Original Data from the Glioma International Case-Control Study and a Meta-analysis. Amirian E Susan,Ostrom Quinn T,Armstrong Georgina N,Lai Rose K,Gu Xiangjun,Jacobs Daniel I,Jalali Ali,Claus Elizabeth B,Barnholtz-Sloan Jill S,Il'yasova Dora,Schildkraut Joellen M,Ali-Osman Francis,Sadetzki Siegal,Jenkins Robert B,Lachance Daniel H,Olson Sara H,Bernstein Jonine L,Merrell Ryan T,Wrensch Margaret R,Johansen Christoffer,Houlston Richard S,Scheurer Michael E,Shete Sanjay,Amos Christopher I,Melin Beatrice,Bondy Melissa L Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology BACKGROUND:There have been few studies of sufficient size to address the relationship between glioma risk and the use of aspirin or NSAIDs, and results have been conflicting. The purpose of this study was to examine the associations between glioma and aspirin/NSAID use, and to aggregate these findings with prior published studies using meta-analysis. METHODS:The Glioma International Case-Control Study (GICC) consists of 4,533 glioma cases and 4,171 controls recruited from 2010 to 2013. Interviews were conducted using a standardized questionnaire to obtain information on aspirin/NSAID use. We examined history of regular use for ≥6 months and duration-response. Restricted maximum likelihood meta-regression models were used to aggregate site-specific estimates, and to combine GICC estimates with previously published studies. RESULTS:A history of daily aspirin use for ≥6 months was associated with a 38% lower glioma risk, compared with not having a history of daily use [adjusted meta-OR = 0.62; 95% confidence interval (CI), 0.54-0.70]. There was a significant duration-response trend ( = 1.67 × 10), with lower ORs for increasing duration of aspirin use. Duration-response trends were not observed for NSAID use. In the meta-analysis aggregating GICC data with five previous studies, there was a marginally significant association between use of aspirin and glioma (mOR = 0.84; 95% CI, 0.70-1.02), but no association for NSAID use. CONCLUSIONS:Our study suggests that aspirin may be associated with a reduced risk of glioma. IMPACT:These results imply that aspirin use may be associated with decreased glioma risk. Further research examining the association between aspirin use and glioma risk is warranted. 10.1158/1055-9965.EPI-18-0702
    Early life exposures and the risk of adult glioma. Anic Gabriella M,Madden Melissa H,Sincich Kelly,Thompson Reid C,Nabors L Burton,Olson Jeffrey J,LaRocca Renato V,Browning James E,Pan Edward,Egan Kathleen M European journal of epidemiology Exposure to common infections in early life may stimulate immune development and reduce the risk for developing cancer. Birth order and family size are proxies for the timing of exposure to childhood infections with several studies showing a reduced risk of glioma associated with a higher order of birth (and presumed younger age at infection). The aim of this study was to examine whether birth order, family size, and other early life exposures are associated with the risk of glioma in adults using data collected in a large clinic-based US case-control study including 889 glioma cases and 903 community controls. A structured interviewer-administered questionnaire was used to collect information on family structure, childhood exposures and other potential risk factors. Logistic regression was used to calculate odds ratios (OR) and corresponding 95% confidence intervals (CI) for the association between early life factors and glioma risk. Persons having any siblings were at significantly lower risk for glioma when compared to those reporting no siblings (OR=0.64; 95% CI 0.44-0.93; p=0.020). Compared to first-borns, individuals with older siblings had a significantly lower risk (OR=0.75; 95% CI 0.61-0.91; p=0.004). Birth weight, having been breast fed in infancy, and season of birth were not associated with glioma risk. The current findings lend further support to a growing body of evidence that early exposure to childhood infections reduces the risk of glioma onset in children and adults. 10.1007/s10654-013-9811-1
    Glioma in Schizophrenia: Is the Risk Higher or Lower? Gao Xingchun,Mi Yajing,Guo Na,Xu Hao,Jiang Pengtao,Zhang Ruisan,Xu Lixian,Gou Xingchun Frontiers in cellular neuroscience Whether persons with schizophrenia have a higher or lower incidence of cancer has been discussed for a long time. Due to the complex mechanisms and characteristics of different types of cancer, it is difficult to evaluate the exact relationship between cancers and schizophrenia without considering the type of tumor. Schizophrenia, a disabling mental illness that is now recognized as a neurodevelopmental disorder, is more correlated with brain tumors, such as glioma, than other types of tumors. Thus, we mainly focused on the relationship between schizophrenia and glioma morbidity. Glioma tumorigenesis and schizophrenia may share similar mechanisms; gene/pathway disruption would affect neurodevelopment and reduce the risk of glioma. The molecular defects of disrupted-in-schizophrenia-1 (DISC1), P53, brain-derived neurotrophic factor (BDNF) and C-X-C chemokine receptors type 4 (CXCR4) involved in schizophrenia pathogenesis might play opposite roles in glioma development. Many microRNAs (miRNAs) such as miR-183, miR-9, miR-137 and miR-126 expression change may be involved in the cross talk between glioma prevalence and schizophrenia. Finally, antipsychotic drugs may have antitumor effects. All these factors show that persons with schizophrenia have a decreased incidence of glioma; therefore, epidemiological investigation and studies comparing genetic and epigenetic aberrations involved in both of these complex diseases should be performed. These studies can provide more insightful knowledge about glioma and schizophrenia pathophysiology and help to determine the target/strategies for the prevention and treatment of the two diseases. 10.3389/fncel.2018.00289
    Lack of association between modifiable exposures and glioma risk: a Mendelian randomization analysis. Saunders Charlie N,Cornish Alex J,Kinnersley Ben,Law Philip J,Claus Elizabeth B,Il'yasova Dora,Schildkraut Joellen,Barnholtz-Sloan Jill S,Olson Sara H,Bernstein Jonine L,Lai Rose K,Chanock Stephen,Rajaraman Preetha,Johansen Christoffer,Jenkins Robert B,Melin Beatrice S,Wrensch Margaret R,Sanson Marc,Bondy Melissa L,Houlston Richard S Neuro-oncology BACKGROUND:The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (MR) framework to examine if lifestyle, cardiometabolic, and inflammatory factors influence the risk of glioma. This methodology reduces bias from confounding and is not affected by reverse causation. METHODS:We identified genetic instruments for 37 potentially modifiable risk factors and evaluated their association with glioma risk using data from a genome-wide association study of 12 488 glioma patients and 18 169 controls. We used the estimated odds ratio of glioma associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures:Lifestyle and dietary factors-height, plasma insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A;Cardiometabolic factors-birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; andInflammatory factors- C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E. RESULTS:After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, PCorrected > 0.05). CONCLUSIONS:This study did not provide evidence supporting any of the 37 factors examined as having a significant influence on glioma risk. 10.1093/neuonc/noz209
    Season of birth and risk for adult onset glioma. Efird Jimmy T International journal of environmental research and public health Adult onset glioma is a rare cancer which occurs more frequently in Caucasians than African Americans, and in men than women. The etiology of this disease is largely unknown. Exposure to ionizing radiation is the only well established environmental risk factor, and this factor explains only a small percentage of cases. Several recent studies have reported an association between season of birth and glioma risk. This paper reviews the plausibility of evidence focusing on the seasonal interrelation of farming, allergies, viruses, vitamin D, diet, birth weight, and handedness. To date, a convincing explanation for the occurrence of adult gliomas decades after a seasonal exposure at birth remains elusive. 10.3390/ijerph7051913
    Anthropometric factors in relation to risk of glioma. Little Rebecca B,Madden Melissa H,Thompson Reid C,Olson Jeffrey J,Larocca Renato V,Pan Edward,Browning James E,Egan Kathleen M,Nabors L Burton Cancer causes & control : CCC INTRODUCTION:Increased height and greater adiposity have been linked to an increased risk of many cancer types, though few large studies have examined these associations in glioma. We examined body weight and height as potential risk factors for glioma in a large US-based case-control study. METHODS:The analysis included 1,111 glioma cases and 1,096 community controls. In a structured interview, participants reported their height and weight at 21 years of age, lowest and highest weight in adulthood, and weight 1-5 years in the past. RESULTS:Being underweight at age 21 (BMI < 18.5 kg/m(2)) was inversely associated with the risk of glioma development. This protective association was observed in both men and women, but reached statistical significance in women only (multivariate OR 0.68; 95 % CI 0.48, 0.96). When BMI at age 21 was assessed as a continuous variate, a small but significant increase in risk was observed per unit increase in kg/m(2) (OR 1.04; 95 % CI 1.02, 1.07). Adult height, recent body weight, and weight change in adulthood were not associated with glioma risk. All results were similar among never smokers and were consistent after stratifying by glioma subtype. CONCLUSION:The present data suggest that a low body weight in early adulthood is associated with a reduced risk of glioma later in life. Results are consistent with previous studies in showing no material association of glioma risk with usual adult body weight. The present study does not support any association of adult stature with glioma risk. 10.1007/s10552-013-0178-0
    Relationship between circulating inflammatory factors and glioma risk and prognosis: A meta-analysis. Feng Yuan,Wang Jia,Tan Dezhong,Cheng Peng,Wu Anhua Cancer medicine BACKGROUND:Inflammatory factors have been considered a significant factor contributing to the development and progression of glioma. However, the relationship between circulating inflammatory factors and glioma risk as well as their prognostic values in glioma patients is still inconclusive. Here, we performed a meta-analysis to address this issue. METHODS:Relevant articles were identified through PubMed, EMBASE, the Cochrane Library, Web of Science, Wanfang database, and China National Knowledge Infrastructure (CNKI) from inception to February 2019. The weighted mean differences (WMDs) or standard mean differences (SMDs) with 95% confidence intervals (CIs) were used to describe the predictive ability of the levels of circulating inflammatory factors on glioma risk. To evaluate the prognostic values of the circulating inflammatory factors in glioma, hazard ratios (HRs) with 95% CIs were used. RESULTS:Thirty-one studies comprising 2587 patients were included. The overall analysis showed that increased circulating interleukin-6 (IL-6) [SMD 0.81 (95% CI: 0.21-1.40; P = .008)], interleukin-8 (IL-8) [SMD 1.01 (95% CI: 0.17-1.84; P = .018)], interleukin-17 (IL-17) [SMD 1.12 (95% CI: 0.26-1.98; P = .011)], tumor necrosis factor-α (TNF-α) [SMD 1.80 (95% CI: 1.03-2.56; P = .000)], transforming growth factor-β (TGF-β) [SMD 10.55 (95% CI: 5.59-15.51; P = .000)], and C-reactive protein (CRP) [SMD 0.95 (95% CI: 0.75-1.15; P = .000)] levels were significantly associated with glioma risk. On the other hand, our results showed that circulating IL-6 [HR 1.10 (95% CI: 1.05-1.16; P = .000)] and CRP [HR 2.02 (95% CI: 1.52-2.68; P = .000)] levels were highly correlated with a poor overall survival (OS) rate in glioma patients. CONCLUSION:Our results indicate that increased circulating IL-6, IL-8, IL-17, TNF-α, TGF-β, and CRP levels are significantly associated with increased glioma risk. Moreover, our meta-analysis suggests that circulating IL-6 and CRP may serve as powerful biomarkers for a poor prognosis in glioma patients. 10.1002/cam4.2585
    Impact of atopy on risk of glioma: a Mendelian randomisation study. Disney-Hogg Linden,Cornish Alex J,Sud Amit,Law Philip J,Kinnersley Ben,Jacobs Daniel I,Ostrom Quinn T,Labreche Karim,Eckel-Passow Jeanette E,Armstrong Georgina N,Claus Elizabeth B,Il'yasova Dora,Schildkraut Joellen,Barnholtz-Sloan Jill S,Olson Sara H,Bernstein Jonine L,Lai Rose K,Schoemaker Minouk J,Simon Matthias,Hoffmann Per,Nöthen Markus M,Jöckel Karl-Heinz,Chanock Stephen,Rajaraman Preetha,Johansen Christoffer,Jenkins Robert B,Melin Beatrice S,Wrensch Margaret R,Sanson Marc,Bondy Melissa L,Houlston Richard S BMC medicine BACKGROUND:An inverse relationship between allergies with glioma risk has been reported in several but not all epidemiological observational studies. We performed an analysis of genetic variants associated with atopy to assess the relationship with glioma risk using Mendelian randomisation (MR), an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations. METHODS:Two-sample MR was undertaken using genome-wide association study data. We used single nucleotide polymorphisms (SNPs) associated with atopic dermatitis, asthma and hay fever, IgE levels, and self-reported allergy as instrumental variables. We calculated MR estimates for the odds ratio (OR) for each risk factor with glioma using SNP-glioma estimates from 12,488 cases and 18,169 controls, using inverse-variance weighting (IVW), maximum likelihood estimation (MLE), weighted median estimate (WME) and mode-based estimate (MBE) methods. Violation of MR assumptions due to directional pleiotropy were sought using MR-Egger regression and HEIDI-outlier analysis. RESULTS:Under IVW, MLE, WME and MBE methods, associations between glioma risk with asthma and hay fever, self-reported allergy and IgE levels were non-significant. An inverse relationship between atopic dermatitis and glioma risk was found by IVW (OR 0.96, 95% confidence interval (CI) 0.93-1.00, P = 0.041) and MLE (OR 0.96, 95% CI 0.94-0.99, P = 0.003), but not by WME (OR 0.96, 95% CI 0.91-1.01, P = 0.114) or MBE (OR 0.97, 95% CI 0.92-1.02, P = 0.194). CONCLUSIONS:Our investigation does not provide strong evidence for relationship between atopy and the risk of developing glioma, but findings do not preclude a small effect in relation to atopic dermatitis. Our analysis also serves to illustrate the value of using several MR methods to derive robust conclusions. 10.1186/s12916-018-1027-5
    Associations of high-grade glioma with glioma risk alleles and histories of allergy and smoking. Lachance Daniel H,Yang Ping,Johnson Derek R,Decker Paul A,Kollmeyer Thomas M,McCoy Lucie S,Rice Terri,Xiao Yuanyuan,Ali-Osman Francis,Wang Frances,Stoddard Shawn M,Sprau Debra J,Kosel Matthew L,Wiencke John K,Wiemels Joseph L,Patoka Joseph S,Davis Faith,McCarthy Bridget,Rynearson Amanda L,Worra Joel B,Fridley Brooke L,O'Neill Brian Patrick,Buckner Jan C,Il'yasova Dora,Jenkins Robert B,Wrensch Margaret R American journal of epidemiology Glioma risk has consistently been inversely associated with allergy history but not with smoking history despite putative biologic plausibility. Data from 855 high-grade glioma cases and 1,160 controls from 4 geographic regions of the United States during 1997-2008 were analyzed for interactions between allergy and smoking histories and inherited variants in 5 established glioma risk regions: 5p15.3 (TERT), 8q24.21 (CCDC26/MLZE), 9p21.3 (CDKN2B), 11q23.3 (PHLDB1/DDX6), and 20q13.3 (RTEL1). The inverse relation between allergy and glioma was stronger among those who did not (odds ratio(allergy-glioma) = 0.40, 95% confidence interval: 0.28, 0.58) versus those who did (odds ratio(allergy-glioma) = 0.76, 95% confidence interval: 0.59, 0.97; P(interaction) = 0.02) carry the 9p21.3 risk allele. However, the inverse association with allergy was stronger among those who carried (odds ratio(allergy-glioma) = 0.44, 95% confidence interval: 0.29, 0.68) versus those who did not carry (odds ratio(allergy-glioma) = 0.68, 95% confidence interval: 0.54, 0.86) the 20q13.3 glioma risk allele, but this interaction was not statistically significant (P = 0.14). No relation was observed between glioma risk and smoking (odds ratio = 0.92, 95% confidence interval: 0.77, 1.10; P = 0.37), and there were no interactions for glioma risk of smoking history with any of the risk alleles. The authors' observations are consistent with a recent report that the inherited glioma risk variants in chromosome regions 9p21.3 and 20q13.3 may modify the inverse association of allergy and glioma. 10.1093/aje/kwr124
    Use of cardiac glycosides and risk of glioma. Seliger Corinna,Meier Christoph R,Jick Susan S,Uhl Martin,Bogdahn Ulrich,Hau Peter,Leitzmann M F Journal of neuro-oncology Cardiac glycosides induce apoptotic effects on glioma cells, but whether cardiac glycosides protect against risk for glioma is unknown. We therefore explored the relation between glycoside use and glioma risk using a large and validated database. We performed a case-control analysis using the Clinical Practice Research Datalink involving 2005 glioma cases diagnosed between 1995 and 2012 that were individually matched to 20,050 controls on age, gender, general practice, and number of years of active history in the database. Conditional logistic regression analysis was used to evaluate the association between cardiac glycosides and the risk of glioma adjusting for body mass index and smoking. We also examined use of common heart failure and arrhythmia medications to differentiate between a specific glycoside effect and a generic effect of treatment for congestive heart failure or arrhythmia. Cardiac glycoside use was inversely related to glioma incidence. After adjustment for congestive heart failure, arrhythmia, diabetes, and common medications used to treat those conditions, the OR of glioma was 0.47 (95% CI 0.27-0.81, Bonferroni-corrected p value = 0.024) for use versus non-use of cardiac glycosides, based on 17 exposed cases. In contrast, no associations were noted for other medications used to treat congestive heart failure or arrhythmias. The OR of glioma in people with congestive heart failure was 0.65 (95% CI 0.40-1.04), and for arrhythmia it was 1.01 (95% CI 0.78-1.31). These data indicate that cardiac glycoside use is independently associated with reduced glioma risk. 10.1007/s11060-015-2036-2
    Prospective study of sleep duration and glioma risk. Samanic Claudine M,Cote David J,Creed Jordan H,Stampfer Meir J,Wang Molin,Smith-Warner Stephanie A,Egan Kathleen M Cancer causes & control : CCC PURPOSE:Both long and short sleep duration have been linked with risk of some cancers, but evidence for glioma is lacking. METHODS:Using prospective data from the UK Biobank (UKB), the Nurses' Health Study (NHS), and the Health Professionals Follow-Up Study (HPFS), we examined the association between self-reported hours of sleep and incident glioma in multivariable-adjusted Cox proportional hazards models. RESULTS:In the UKB, compared to 7 h, sleep durations of < 7 h (HR = 0.90; 95% CI 0.70-1.16) or > 7 h (HR = 1.05; 95% CI 0.85-1.30) were not significantly associated with glioma risk. Likewise, no significant associations were found between sleep duration and glioma risk in the NHS/HPFS for either < 7 h (HR = 0.93; 95% CI 0.69-1.26) or > 7 h (HR = 1.22; 95% CI 0.94-1.57), compared to 7 h. Results were similar for low-grade and high-grade glioma, did not materially change after lagging 2 years, or after accounting for factors known to disrupt sleep. CONCLUSION:Sleep duration was not associated with incident glioma in either the UKB or the NHS/HPFS cohorts. 10.1007/s10552-021-01447-9
    Diabetes mellitus might be a protective factor of glioma. Ni Ting-Ting Journal of cancer research and therapeutics Aims:Several studies suggested that diabetes mellitus (DM) was associated with the risk of glioma. However, other studies did not confirm the result. Therefore, I conducted this meta-analysis. Materials and Methods:I retrieved the PubMed, Embase, and Web of Science database, by adopting keywords "glioma," and "diabetes," "DM." The strength of the associations between DM and the risk of glioma was measured by odds ratios (ORs) with 95% confidence intervals (95% CIs). Results:Ten relevant studies were identified in the final analysis. A statistically significant association between DM and glioma risk was fond (OR = 0.84; 95% CI, 0.73-0.97; P = 0.02). In the subgroup analysis of age group, young population with DM showed decreased glioma risk (OR = 0.83; 95% CI, 0.70-0.98; P = 0.02), whereas old population with DM did not show a significant association (OR = 0.87; 95% CI, 0.65-1.16; P = 0.34). In the subgroup analysis of gender, male patients with DM showed decreased glioma risk (OR = 0.82; 95% CI, 0.68-0.99; P = 0.04), whereas female population with DM did not show a significant association (OR = 0.93; 95% CI, 0.70-1.24; P = 0.63). Conclusions:This meta-analysis suggested that DM may be associated with the reduced glioma risk. 10.4103/0973-1482.183184
    Handedness and the risk of glioma. Miller Briana,Peeri Noah C,Nabors Louis Burt,Creed Jordan H,Thompson Zachary J,Rozmeski Carrie M,LaRocca Renato V,Chowdhary Sajeel,Olson Jeffrey J,Thompson Reid C,Egan Kathleen M Journal of neuro-oncology Gliomas are the most common type of malignant primary brain tumor and few risk factors have been linked to their development. Handedness has been associated with several pathologic neurological conditions such as schizophrenia, autism, and epilepsy, but few studies have evaluated a connection between handedness and risk of glioma. In this study, we examined the relationship between handedness and glioma risk in a large case-control study (1849 glioma cases and 1354 healthy controls) and a prospective cohort study (326,475 subjects with 375 incident gliomas). In the case-control study, we found a significant inverse association between left handedness and glioma risk, with left-handed persons exhibiting a 35% reduction in the risk of developing glioma [odds ratio (OR) = 0.65, 95% confidence interval (CI) 0.51-0.83] after adjustment for age, gender, race, education, and state of residence; similar inverse associations were observed for GBM (OR = 0.69, 95% CI 0.52-0.91), and non-GBM (OR = 0.59, 95% CI 0.42-0.82) subgroups. The association was consistent in both males and females, and across age strata, and was observed in both glioblastoma and in lower grade tumors. In the prospective cohort study, we found no association between handedness and glioma risk (hazards ratio = 0.92, 95% CI 0.67-1.28) adjusting for age, gender, and race. Further studies on this association may help to elucidate mechanisms of pathogenesis in glioma. 10.1007/s11060-018-2759-y
    Statin use, hyperlipidemia, and risk of glioma. Cote David J,Rosner Bernard A,Smith-Warner Stephanie A,Egan Kathleen M,Stampfer Meir J European journal of epidemiology Background Statins have previously been shown to have protective effects for other cancers, but no prospective studies of statin use and glioma have been conducted. Methods We evaluated the association between statin use and risk of glioma in the female Nurses' Health Study (NHS, n = 114,419) and Nurses' Health Study II (NHSII, n = 115,813) and the male Health Professionals Follow-up Study (HPFS, n = 50,223). Glioma cases were confirmed by medical record review. Age and multivariable-adjusted hazard ratios of glioma by statin use were estimated using Cox proportional hazards models. Results In 4,430,700 person-years of follow-up, we confirmed 483 incident cases of glioma. Compared with never-users, ever statin use was associated with borderline increased risk of glioma in the combined cohorts (age-adjusted HR = 1.23, 95% CI 0.99-1.54), as was longer duration of statin use (HR = 1.48, 95% CI 1.08-2.03 comparing > 8 years of use to never use, p-trend = 0.01). We also observed a significant inverse association between hyperlipidemia and glioma in multivariable models (HR = 0.74, 95% CI 0.59-0.93 in combined cohorts), which was attenuated in lagged analyses. Compared to never use, in multivariable-adjusted models, ever statin use (HR = 1.43, 95% CI 1.10-1.86) and statin use duration (HR = 1.72, 95% CI 1.21-2.45, for > 8 years of use, p-trend = 0.003) were each significantly associated with increased glioma risk. Conclusion In contrast to case-control studies reporting inverse associations, we found borderline increased risk of glioma with statin use. Results were strengthened after adjustment for cardiovascular risk factors due to an unexpected inverse association between hyperlipidemia and glioma risk. Further studies of statin use, hyperlipidemia, and glioma risk are warranted. 10.1007/s10654-019-00565-8