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.
We offer iDDS assays for common APC, BRAF, and CTNNB1 mutations. We also offer a dual-iDDS probe assays for simultaneous negative detection of several KRAS mutations