What you carry at this position in your DNA and what research says about it.
Brain Tumor Risk: 10/10 evidence, 19 publications.
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Sample genotype (not yours): A/A
Typical Brain Tumor Risk
Carrying two copies of the common A allele is associated with a typical, baseline risk of developing brain tumors. This genotype represents the standard genetic profile found in the vast majority of the population.
What this genotype means: Typical baseline risk of glioma; Standard brain white matter structure.
Sample genotype (not yours): A/G
6x Increased Glioma Risk
Carrying one copy of the G allele is associated with a significantly higher relative risk of developing a specific subtype of brain tumor. However, because these tumors are rare, the absolute risk remains very low.
What this genotype means: Elevated relative risk of IDH-mutant glioma; Altered brain white matter measurements.
Sample genotype (not yours): G/G
Carrying two copies of the G allele is associated with an elevated relative risk of developing IDH-mutant brain tumors. The absolute risk of developing these rare tumors remains very low.
Gene function and biological role
Gene Function: CCDC26 encodes a long non-coding RNA located on chromosome 8q24.21 [1]. This gene does not produce a protein, but instead functions as a molecular regulator of other genes [2]. Research indicates that CCDC26 plays a critical role in cellular differentiation and the regulation of cell growth [1]. In particular, it is highly active in the brain and interacts with key oncogenes like MYC [2]. Alterations in this gene regulatory region are heavily studied for their strong links to brain tumor development [1].
Variant Impact: The rs55705857 variant is an intronic single nucleotide change within the CCDC26 gene [1]. This genetic alteration acts as a powerful enhancer that selectively increases the expression of the MYC oncogene in brain cells [2]. By altering the local chromatin structure, the variant facilitates the acquisition of somatic IDH1 or IDH2 mutations during early tumor development [2]. It represents one of the strongest inherited risk factors discovered for any cancer type [1]. Despite this strong relative risk, the absolute risk of developing a brain tumor remains low because these cancers are rare overall [1].
Key Insight: This variant is one of the strongest inherited risk factors ever discovered for any cancer, yet the absolute risk remains very low because brain tumors are rare.
Location: CCDC26. Chromosome 8 · 8q24.21 · 129.6 Mb
Estimated prevalence by population
Global 92.6%; European 89.1%; African 98.1%; East Asian 99.8%; South Asian 95.5%; Americas 96.2%; Ashkenazi 97.1%; Finnish 82.0%; Middle Eastern 98.0%; Amish 95.2%.
Estimated AA genotype frequency.
Global 7.2%; European 10.6%; African 1.9%; East Asian 0.2%; South Asian 4.5%; Americas 3.8%; Ashkenazi 2.9%; Finnish 17.1%; Middle Eastern 2.0%; Amish 4.7%.
Estimated AG genotype frequency.
Global 0.2%; European 0.3%; African < 0.1%; East Asian < 0.1%; South Asian 0.1%; Americas < 0.1%; Ashkenazi < 0.1%; Finnish 0.9%; Middle Eastern < 0.1%; Amish 0.1%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cancer & Oncology
Brain & Nervous System Cancers
Glioma. Evidence: 10/10. Source: PMID 28346443. Typical Risk.
Brain Cancer. Evidence: 8/10. Source: PMID 26424050. Typical Risk.
Glioblastoma. Evidence: 8/10. Source: PMID 28346443. Typical Risk.
Neurology & Mental Health
Neurodevelopmental Traits
Brain White Matter. Evidence: 6/10. Source: PMID 33875891. Typical Structure.
Showing effects for A/G genotype
Glioma. Evidence: 10/10. Source: PMID 28346443. ~6x Increased Risk.
Brain Cancer. Evidence: 8/10. Source: PMID 26424050. Increased Risk.
Glioblastoma. Evidence: 8/10. Source: PMID 28346443. Increased Risk.
Brain White Matter. Evidence: 6/10. Source: PMID 33875891. Altered Structure.
Showing effects for G/G genotype
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Inheriting two copies of the ancestral A allele means lacking the genetic enhancer that drives MYC oncogene overactivation in glial cells [1]. Large-scale genome-wide association studies show that this typical profile is protective against the development of IDH-mutant gliomas compared to carrying the G allele [1]. The absolute risk of developing these rare brain tumors remains extremely low, at approximately 2 to 3 cases per 100,000 people annually [2]. Brain imaging studies also suggest that this genotype is associated with normal variations in white matter microstructure and brain connectivity [3]. No special medical screening or interventions are recommended for individuals with this standard genetic baseline.
Typical baseline risk of glioma; Standard brain white matter structure.
Sample genotype: AG (Heterozygous)
Inheriting a single copy of the G allele introduces a powerful genetic enhancer that deregulates MYC signaling in brain tissues [1]. Clinical studies demonstrate that this variant is strongly linked to a 5- to 6-fold increase in the relative risk of developing IDH-mutant gliomas [2]. Despite this high relative risk, the absolute lifetime probability of developing a glioma remains under 1% because these brain cancers are rare in the general population [2]. Interestingly, some research suggests that among patients who do develop certain low-grade gliomas, carriers of this variant may experience different survival outcomes depending on the specific tumor subtype [3]. This genetic marker is a susceptibility factor, not a direct diagnosis, and does not guarantee that a tumor will ever form.
Elevated relative risk of IDH-mutant glioma; Altered brain white matter measurements.
Sample genotype: GG (Homozygous)
Inheriting two copies of the G risk allele creates a highly active enhancer state that promotes MYC oncogene expression in glial cells [1]. This genotype is associated with a 5- to 6-fold increase in the relative risk of developing IDH-mutant gliomas and oligodendrogliomas [2]. Because brain tumors are rare, the vast majority of individuals with this genetic profile will never develop a tumor in their lifetime [2]. Researchers use this variant to study the early molecular pathways that lead to brain tumor initiation [1]. Having this genotype is not a medical diagnosis and does not warrant preemptive clinical screening under current guidelines.
Variants with shared genetic architecture
rs1991866 · CCDC26 Gene · Chr 8 · IBD and Blood Traits
rs4295627 · CCDC26 Gene · Chr 8 · Brain Tumor Risk
rs6010620 · RTEL1 Gene · Chr 20 · Glioma and Eczema Risk
A noncoding single-nucleotide polymorphism at 8q24 drives IDH1-mutant glioma formation.
An expanded set of genome-wide association studies of brain imaging phenotypes in UK Biobank.
Content updated August 2026.
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