BS1 strong: gnomAD v4.1 Popmax FAF of 1.064e-05 exceeds the APC VCEP threshold of 1e-05. BP1 supporting: residue 2532 lies outside the APC VCEP exception at codons 1021-1035.
APC is a tumor suppressor gene whose protein acts as a key brake on the Wnt signaling pathway by helping mark the growth-promoting protein beta-catenin for destruction; it also participates in cell migration, adhesion, and apoptosis. Inherited mutations in APC cause familial adenomatous polyposis (FAP), an autosomal dominant condition characterized by numerous colorectal polyps and a very high risk of colorectal cancer, with related forms including attenuated FAP and gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS). Somatic APC mutations are found in roughly 50-80% of sporadic colorectal cancers, where they act as early tumor-initiating events, and are also observed in some breast, stomach, and prostate cancers. Loss of APC function leaves Wnt signaling abnormally active, driving uncontrolled cell growth, which makes APC a central tumor suppressor in colorectal cancer.
The APC p.(His2532Tyr) missense change is evaluated in the context of APC's tumor-suppressor role in restraining Wnt signaling and its association with autosomal-dominant familial adenomatous polyposis.
BS1 strong: gnomAD v4.1 Popmax FAF of 1.064e-05 exceeds the APC VCEP threshold of 1e-05. BP1 supporting: residue 2532 lies outside the APC VCEP exception at codons 1021-1035.
African/African American 3 / 74,892 |
0.004% |
Remaining individuals 1 / 62,464 |
0.0016% |
European (non-Finnish) 18 / 1,179,330 |
0.0015% |
African/African American 1 / 24,964 |
0.004% |
European (non-Finnish) 4 / 128,496 |
0.0031% |