What genetic mutation is associated with familial adenomatous polyposis (FAP)?

Familial adenomatous polyposis (FAP) is a hereditary condition characterized by the development of numerous colorectal polyps and a high risk for colorectal cancer. The condition is primarily caused by mutations in the adenomatous polyposis coli (APC) gene.

The APC gene is a tumor suppressor gene that plays a critical role in regulating cell growth and adhesion. When there is a mutation in this gene, it leads to uncontrolled cell proliferation, resulting in the formation of polyps in the colon and rectum. These polyps have a high tendency to become malignant over time, underscoring the importance of early detection and management in individuals with FAP.

In contrast, mutations in the other genes listed, such as BRCA1, P53, and KRAS, are associated with different types of cancers and syndromes. BRCA1 is primarily linked to breast and ovarian cancers, P53 mutations are often associated with a broad range of cancers due to its role in the cell cycle and apoptosis, and KRAS mutations are commonly found in various cancers, especially pancreatic cancer. However, none of these genes are involved in the pathogenesis of familial adenomatous polyposis.

Thus, a mutation in the APC gene