iDDS probe assays for APC, BRAF, CTNNB1, and KRAS mutations

Mutually exclusive KRAS and BRAF driver mutations activate the CTNNB1 protein, which promotes colorectal tumor growth and invasion. Activating CTNNB1 mutations gene drive overexpression of proto-oncogenes such as c-Myc. In contrast, signaling through the Wnt and APC proteins causes CTNNB1 protein degradation. Thus, APC mutations are common in colorectal cancer (~70% of all cases) and often arise as the first driver mutations. In addition, CTNNB1, KRAS, and BRAF mutations have been identified in ~80%, 40%, and 10% of colorectal cancers, respectively.