Adenomatous Polyposis Coli is (APC) serves as a key tumor suppressor gene by suppressing canonical Wnt signaling pathway which is essential for tumorigenesis. Mutation in APC has been observed in more that 80% of colorectal cancers and more than 90% of these mutations result in the production of truncated proteins. Germline mutation in APC results in an inherited disorder called Familial Adenomatous Polyposis (FAP), characterized by the development of multiple benign polyps in the colon that eventually, with the age, become malignant. Although mutation in APC has been well characterized in colorectal cancers, several studies and databases have shown its varied expression levels in other cancers as well.
Due to the clinical importance, mutation in APC or its expression have been studied extensively. APC has diverse cellular functions that are required for the maintenance of cellular homeostasis to prevent tumorigenesis. Hence, a part of our study is to report whether there is an association between a pathway that involves APC and cancer progression. Another part of our study involves studying mutational and expression profile of APC and their association with cancers.
Roshan L. Shrestha, PhD
Aroj Hada, Research Intern, 4th Year B. Tech. Biotechnology, Kathmandu University
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