PM2 supporting: the variant is extremely rare in gnomAD, with non-cancer AF 6.75776e-06. BP4 supporting: SpliceAI maximum delta 0.084 is below the <=0.1 benign threshold.
This variant was interpreted by pipeline 8.0.0. The current version is 10.0.0. Re-running queues a fresh interpretation; the result replaces this page when complete.
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POLE encodes the catalytic subunit of DNA polymerase epsilon, the enzyme that replicates the leading strand of DNA during cell division and participates in DNA repair. It contains a proofreading domain that corrects replication errors, keeping the accumulation of mutations in check. Germline mutations in POLE cause polyposis and predispose to colorectal cancer, and are also linked to a rare syndrome of facial dysmorphism, immunodeficiency, livedo, and short stature. Somatic mutations, particularly in the proofreading domain, occur in colorectal and endometrial cancers, where they drive an ultra-mutated tumor phenotype and are associated with better responses to immune checkpoint inhibitors.
The variant lies in POLE, which encodes the DNA polymerase epsilon catalytic subunit involved in leading-strand replication and DNA repair and is implicated in inherited polyposis and colorectal-cancer predisposition.
PM2 supporting: the variant is extremely rare in gnomAD, with non-cancer AF 6.75776e-06. BP4 supporting: SpliceAI maximum delta 0.084 is below the <=0.1 benign threshold.
Remaining individuals 3 / 62,480 |
0.0048% |
African/African American 2 / 74,932 |
0.0027% |
East Asian 1 / 44,886 |
0.0022% |
Admixed American 1 / 60,002 |
0.0017% |
East Asian 2 / 18,394 |
0.011% |
East Asian 6 / 1,338 |
0.45% |