Role of APC and DNA mismatch repair genes in the development of colorectal cancers

Satya Narayan¹ and Deodutta Roy²

¹Department of Anatomy and Cell Biology and UF Shands Cancer Center, College of Medicine, Academic Research Building, Room R4-216, 1600 SW Archer Road, University of Florida, Gainesville, FL 32610, USA

²Environmental Health Sciences, University of Alabama at Birmingham, 317 Ryals Building, 1665 University Boulevard, Birmingham, AL 35294-0022, USA

author email corresponding author email

Molecular Cancer 2003, 2:41doi:10.1186/1476-4598-2-41


Published:	12 December 2003

Abstract

Colorectal cancer is the third most common cause of cancer-related death in both men and women in the western hemisphere. According to the American Cancer Society, an estimated 105,500 new cases of colon cancer with 57,100 deaths will occur in the U.S. in 2003, accounting for about 10% of cancer deaths. Among the colon cancer patients, hereditary risk contributes approximately 20%. The main inherited colorectal cancers are the familial adenomatous polyposis (FAP) and the hereditary nonpolyposis colorectal cancers (HNPCC). The FAP and HNPCC are caused due to mutations in the adenomatous polyposis coli (APC) and DNA mismatch repair (MMR) genes. The focus of this review is to summarize the functions of APC and MMR gene products in the development of colorectal cancers.