A brain tumor arising from glial cells, about 50% more common in men than women — three studies from 2009 to 2018 found 6 contributing variants, on this page, including one whose effect differs by sex.
Glioma is a type of brain tumor that arises from glial cells, the support cells of the nervous system, ranging from slow-growing to the aggressive glioblastoma (GBM) subtype. Incidence is roughly 50% higher in men than women, a difference genetics only partly explains.
A 2017 meta-analysis of 12,496 cases and 18,190 controls was the first large glioma GWAS to split cases by tumor subtype rather than treating glioma as one disease. It found 5 new loci specific to glioblastoma and 8 new loci specific to non-glioblastoma tumors — evidence the two subtypes have genuinely distinct genetic susceptibility, likely reflecting different underlying biology. This page's rs12752552, near RAVER2, is one of the 5 new GBM-specific loci; rs3751667, in LMF1, is one of the 8 new non-GBM loci.
A 2018 study took a different angle: it combined four earlier glioma GWAS — 4,831 male cases and 5,216 male controls, 3,206 female cases and 5,470 female controls — and analyzed men and women separately, the first glioma GWAS to do so, motivated directly by that ~50% sex gap in incidence. Its headline finding is this page's rs55705857, near MYC at 8q24.21: the association with glioma risk was measurably stronger in women than in men at this exact variant. The same combined dataset also carries this page's rs634537 (CDKN2B-AS1) and rs2297440 (RTEL1); the paper's own sex-difference finding is specifically about the MYC variant, not these two. CDKN2B-AS1 also appears on this site's glaucoma page.
An earlier 2009 meta-analysis — 1,878 cases and 3,670 controls at discovery, 2,545 and 2,953 more at validation — first established the 8q24.21 region, near CCDC26, as a glioma risk locus. This page's rs891835 sits in that same region and gene, from that same paper's association records, though it is not the identical SNP the paper's abstract names as its own top hit there.
Positions joined since this page was written
What this is The text above discusses the variants this page was written around. Since then the catalogue has joined 1 more position to it, by shared trait or shared paper. They are listed here by the paper each came from; the text does not describe them, and each variant page carries that study's own record.
Chen H et al. 2019, International journal of cancer rs10842893 (STK38L) — PMID:30714141
2026-09-17 · Tignor N, Wang P, et al. Cell Reports Medicine. 2026. DOI:10.1016/j.xcrm.2026.103024
Researchers at Icahn School of Medicine at Mount Sinai, with the Clinical Proteomic Tumor Analysis Consortium (CPTAC), the Children's Brain Tumor Network and the Philadelphia Coalition for a Cure, profiled tumor proteins and genetics from 112 high-grade glioma patients aged 83 days to 40 years, combined with 99 adult glioblastoma tumors and clinical data from over 5,000 high-grade glioma cases. High-grade glioma is among the most aggressive primary brain tumors, with a five-year survival rate below 10%. Analyzing molecular profiles continuously across age found a clear shift around age 26, with adolescent (15-26) and young-adult (26-40) tumors relying on distinct signaling programs and showing different survival outcomes -- a finding with real implications for how these age groups should be studied and treated, rather than lumped together. The study also identified four candidate kinase drug targets (CDK8, ATM, ATR, LCK), with CDK8 flagged as particularly notable for being less studied than the other three, and found that about 27% of measured proteins showed sex-different age patterns, with a prognostic score and glycosylation-based survival signal that held up in male patients but not female ones. None of the four candidate kinase genes overlap the genes already catalogued on this page.
Glioma is diagnosed by brain imaging and tissue biopsy, not by any variant on this page. The variants here describe genetic contributors to population-level risk found in large research studies — none is used clinically to screen for glioma or guide its treatment.
Treatment decisions for glioma depend on tumor type, grade, and location, determined by a neuro-oncology team — not by genotype.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Glioma comes down to these specific, well-studied positions — not a diagnosis.
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 14 of 15 linked studies with a resolved discovery ancestry.
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Glioma. MyGeneLog™. https://www.mygenelog.com/conditions/glioma
A type of brain tumor arising from glial cells, the nervous system's support cells, ranging from slow-growing to the aggressive glioblastoma subtype. It's roughly 50% more common in men than women.
Not entirely. A 2017 study found 5 loci specific to glioblastoma and 8 loci specific to non-glioblastoma tumors, evidence the two have genuinely distinct genetic susceptibility.
One does. A 2018 sex-stratified study found that the MYC-region variant on this page has a stronger association with glioma risk in women than in men.
No. Glioma is diagnosed by brain imaging and tissue biopsy, not by any variant listed here.
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