***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: We examined the relation between the use of hormone replacement therapy ( HRT )  and the  incidence of central nervous system ( CNS ) tumours  in a large prospect i ve study of 1,147,894 postmenopausal women . Women were aged 56.6 years on average at entry , and HRT use was recorded at recruitment and up date d , where possible , about 3 years later . During a mean follow‐up of 5.3 years per woman , 1,266 CNS tumours were diagnosed , including 557 gliomas , 311 meningiomas and 117 acoustic neuromas . Compared with never users of HRT , the relative risks ( RRs ) for all incident CNS tumours , gliomas , meningiomas and acoustic neuromas in current users of HRT were 1.20 ( 95 % CI : 1.05–1.36 ) , 1.09 ( 95 % CI : 0.89–1.32 ) , 1.34 ( 95 % CI : 1.03–1.75 ) and 1.58 ( 95 % CI : 1.02–2.45 ) , respectively , and there was no significant difference in the relative risks by tumour type ( heterogeneity p = 0.2 ) . In past users of HRT  the relative risk was 1.07 ( 95 % CI : 0.93–1.24 ) for all CNS tumours . Among current users of HRT , there was significant heterogeneity by the type of HRT  with the users of oestrogen‐only HRT at higher risk of all CNS tumours than users of oestrogen – progestagen HRT ( RR = 1.42 , 95 % CI : 1.21–1.67 versus RR = 0.97 , 95 % CI : 0.82–1.16 ) ( heterogeneity p < 0.001 ) . Among current users of oestrogen‐only and oestrogen – progestagen HRT , there was no significant heterogeneity by duration of use , hormonal constituent or mode of administration of HRT 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 r and omly selected controls stratified on age and geographic region ( n = 1,774 ) in Denmark , Finl and , 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 ; Ptrend 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 . ( Cancer Epidemiol Biomarkers Prev 2008;17(10):2663–70 Several case – control studies have suggested that nonsteroidal anti-inflammatory drugs ( NSAIDs ) reduce risk for glioblastoma , an aggressive form of brain cancer . Prospect i ve investigations have not observed such an association , but these studies lacked adequate brain cancer case numbers and did not stratify by histologic subtype . We prospect ively investigated the association between NSAID use and risk of all glioma as well as the risk of glioblastoma subtype in the National Institutes of Health (NIH)-AARP Diet and Health Study . The frequency of aspirin and nonaspirin NSAID use 1 year prior to baseline was ascertained using a self-administered question naire .  Hazard ratios ( HRs ) and 95 % confidence intervals ( CI ) were estimated using Cox regression models with age as the underlying time metric , adjusted for sex , race , and history of heart disease . The analysis included 302,767 individuals , with 341 incident glioma cases ( 264 glioblastoma ) . No association was observed between regular use ( > 2 times/wk ) of aspirin and risk of glioma ( HR = 1.16 ; 95 % CI , 0.87–1.56 ) or glioblastoma ( HR = 1.17 ; 95 % CI , 0.83–1.64 ) as compared with no use . Null associations were also observed for  nonaspirin NSAID use ( HR for glioma = 0.90 ; 95 % CI , 0.65–1.25 and HR for glioblastoma = 0.83 ; 95 % CI , 0.56–1.20 ) as compared with no use . Our findings from this large prospect i ve study do not support an inverse association between NSAIDs and risk of all glioma or glioblastoma . Cancer Prev Res ; 4(12 ) ; 2027–34 . © 2011 AACR The widespread use of cellular telephones has generated concern about possible adverse health effects , particularly brain tumors . In this population -based case-control study carried out in three regions of Germany , all incident cases of glioma and meningioma among patients aged 30 - 69 years were ascertained during 2000 - 2003 . Controls matched on age , gender , and region were r and omly drawn from population registries . In total , 366 glioma cases , 381 meningioma cases , and 1,494 controls were interviewed . Overall use of a cellular phone was not associated with brain tumor risk ; the respective odds ratios were 0.98 ( 95 % confidence interval ( CI ) : 0.74 , 1.29 ) for glioma and 0.84 ( 95 % CI : 0.62 , 1.13 ) for meningioma . Among persons who had used cellular phones for 10 or more years , increased risk was found for glioma ( odds ratio = 2.20 , 95 % CI : 0.94 , 5.11 ) but not for meningioma ( odds ratio = 1.09 , 95 % CI : 0.35 , 3.37 ) . No excess of temporal glioma ( p = 0.41 ) or meningioma ( p = 0.43 ) was observed in  cellular phone users as compared with nonusers . Cordless phone use was not related to either glioma risk or meningioma risk . In conclusion , no overall increased risk of glioma or meningioma was observed among these cellular phone users ; however , for long-term cellular phone users , results need to be confirmed before firm conclusions can be drawn Few risk factors for meningioma , aside from increasing age and female sex , have been identified . We investigated risk factors for meningioma in elderly women , a group with a high incidence . We evaluated associations of demographic , lifestyle , medical history , and anthropometric variables with risk of meningioma in the Iowa Women 's Health Study ( IWHS ) , a population -based , prospect i ve cohort study . Risk factors were collected via question naires mailed in 1986 and 1992 . Incident meningiomas were identified via linkages to Medicare . Cox regression models were used to examine the association of risk factors with meningioma incidence . The mean age at baseline of the 27,791 women in the analysis cohort was 69.3 years ( range , 65.0 - 84.6 years ) . During 291,021 person-years of follow-up , 125 incident meningiomas were identified . After adjusting for age , lower levels of physical activity ( relative risk [ RR ] , 0.68 for high versus low ; P for trend = .039 ) , greater body mass index ( BMI ; RR , 2.14 for ≥35 versus 19.5 - 24.9 kg/m(2 ) ; P for trend = .0019 ) , greater height ( RR , 2.04 for > 66 versus ≤62 inches ; P for trend = .013 ) , and a history of uterine fibroids ( RR , 1.72 ; 95 % confidence interval , 1.19 , 2.50 ) were positively associated with meningioma risk in multivariate analysis . BMI at age 18 and 30 years were not associated with risk . There were no associations with menstrual or reproductive factors or other medical history and lifestyle factors . Physical activity , BMI , height , and history of uterine fibroids were associated with meningioma risk in older women . The positive association with height suggests a role for early life influences on risk , whereas the associations with BMI and physical activity suggest a role for modifiable factors later in life Background : N-nitroso compounds ( NOC ) are found in processed meat and are formed endogenously from intake of nitrite and nitrate . Endogenous NOC formation is antagonized by nitrosation inhibitors in fruit and vegetables ( e.g. , vitamin C ) and promoted by heme in red meat . It has been hypothesized that a diet result ing in high exposure to NOCs increases adult glioma risk . Methods : Using proportional hazards models , we tested this hypothesis among 545,770 participants in the prospect i ve NIH-AARP Diet and Health Study , which assessed dietary intake  at baseline ( 1995–1996 ) with a comprehensive food frequency question naire , and at ages 12 to 13 years with an abbreviated food frequency question naire . Results : During follow-up through 2003 , 585 participants were diagnosed with glioma . We found no significant trends in glioma risk for consumption of processed or red meat , nitrate , or vitamin C or E. We found significant positive trends for nitrite intake from plant sources ( hazard ratio for quintile 5 versus quintile 1 , 1.59 ; 95 % confidence interval , 1.20–2.10 ; P for trend = 0.028 ) and , unexpectedly , for fruit and vegetable intake ( hazard ratio , 1.42 ; 95 % confidence interval , 1.08–1.86 ; P for trend = 0.0081 ) . Examination of interactions between dietary intakes ( e.g. , nitrite and vitamin C ) and a limited analysis of diet at ages 12 to 13 years provided no support for the NOC hypothesis . Conclusions : Our results suggest that consumption of processed or red meat , nitrite , or nitrate does not increase adult glioma risk , and that consumption of fruit and vegetables , vitamin C , or vitamin E does not reduce risk . Impact : Our results , in agreement with the only previous prospect i ve analysis , cast doubt on the NOC hypothesis in relation to dietary intake and adult glioma risk . Cancer Epidemiol Biomarkers Prev ; 19(7 ) ; 1709–22 . © 2010 AACR BACKGROUND Increased levels of serum immunoglobulin E ( IgE ) because of allergies have been inversely associated with risk of glioma in observational studies . Despite consistency across studies examining history of allergies and glioma , questions remain as to whether those are causal associations . An inverse association between serum IgE and risk of glioma was reported in a large case-control study , but reverse causality and treatment effects remain potential explanations for those findings . METHODS We combined data from four prospect i ve cohort studies and used a nested case-control design to examine the association between allergy and glioma . We included glioma case subjects who were confirmed from medical or pathology records or from death certificates , and with prediagnostic blood available . We matched three control subjects per case subject , and the final numbers for analyses were 169 case subjects and 520 control subjects .  Total IgE , food allergen-specific IgE , and respiratory allergen-specific IgE levels were measured using a highly sensitive fluorescent assay . Odds ratios ( ORs ) and 95 % confidence intervals ( CIs ) were calculated using conditional logistic regression analysis . Stratified analyses were conducted by age and birth cohorts . RESULTS Borderline elevated total IgE levels ( 25 - 100 kU/L ) showed a statistically significant inverse association with glioma ( OR = 0.63 , 95 % CI = 0.42 to 0.93 ) , but no association was noted between elevated IgE ( > 100 kU/L ) and glioma ( OR = 0.98 , 95 % CI = 0.61 to 1.56 ) compared with clinical ly normal IgE levels ( < 25 kU/L ) . The association between glioma and total IgE was consistent for both men and women . Non-statistically significant inverse associations were noted for elevated IgE levels among individuals born before year 1930 ( OR = 0.67 , 95 % CI = 0.34 to 1.34 ) and when restricting analyses to highly fatal ( deceased within 2 years of diagnosis ) glioma case subjects ( OR = 0.64 , 95 % CI = 0.34 to 1.19 ) compared with individuals with clinical ly normal IgE levels . No associations were observed 
    Output:
    
Based on this review , various genetic variants , pesticide exposures , occupational farming/hairdressing , cured meat consumption and personal hair dye use appear to be associated with increased risk of onset amongst adults .
The specific EGF polymorphsm 61‐A allele within Caucasian population s and having a history of allergy was associated with a decreased risk .
For progression , M1B‐1 antigen was shown to increase the risk .
High birth weight , pesticide exposure ( childhood exposure , and parental occupational exposure ) and maternal consumption of cured meat during pregnancy may also increase the risk of onset of childhood brain tumours .
Conversely , maternal intake of pre‐natal supplements ( folic acid ) appeared to decrease risk .