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Many genetic and environmental factors have been explored in epidemiological studies of glioma risk but the magnitude of effect of these factors on gliomagenesis is uncertain. A number of constitutional genes associated with glioma risk, many noted to be related to telomere function, have been identified. High-dose ionizing radiation has consistently been associated with an increased glioma risk while a history of allergies and atopy is inversely associated with risk. Results have been inconsistent for most other factors studied but whether this lack of evidence is due to study limitations or a true lack of risk factors is unclear. Using 901 glioma exomes from The Cancer Genome Atlas (TCGA) we estimate the intensity of positive selection on gene variants, and order them by their cancer effect size, quantifying the contribution of gene variants to the somatic evolution of glioma. Examination of subsets of tumor exomes from males and females showed similar patterns in genes mutated but some differences in variant profile for a given gene including PIK3CA suggesting a possible differential response to treatment. Furthermore, these cancer effect sizes enable quantification of the degree to which COSMIC-defined processes associated with genetic pathways and environmental environmental factors within the somatic evolution of tumors contribute mutations that are highly selected, driving gliomagenesis. The results confirm the major roles of previously reported mutations in IDH1, TP53, EGFR, and PIK3CA, but also suggest a large cancer effect for low-prevalence genes including BRAF. Age-related mutagenesis was the primary molecular signature identified for all glioma while homologous recombination disfunction was an important signature for males but not females. Although additional signatures remain to be identified and less common exposures difficult to access, these data suggest a profile of glioma mutations that are caused primarily from endogenous rather than exogenous factors.

EPID-26. SEX-SPECIFIC GLIOMA MOLECULAR SIGNATURES