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

被引:127
作者
Satya Narayan
Deodutta Roy
机构
[1] Department of Anatomy/Cell Biology, UF Shands Cancer Center, University of Florida, Gainesville, FL 32610
[2] Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294-0022
关键词
Familial Adenomatous Polyposis; Adenomatous Polyposis Coli; Familial Adenomatous Polyposis Patient; Adenomatous Polyposis Coli Gene; Adenomatous Polyposis Coli Protein;
D O I
10.1186/1476-4598-2-41
中图分类号
学科分类号
摘要
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. © 2003 Narayan and Roy; licensee BioMed Ltd.
引用
收藏
页数:15
相关论文
共 143 条
[1]  
Muto T., Bussey H.J., Morson B.C., The evolution of cancer of the colon and rectum, Cancer, 36, pp. 2251-2270, (1995)
[2]  
Fearon E.R., Vogelstein B., A genetic model for colorectal tumorigenesis, Cell, 61, pp. 759-767, (1990)
[3]  
Bodmer B.F., The somatic evolution of cancer. The Harveian Oration of 1996, J. Royal Coll. Physicians Lond., 31, pp. 82-89, (1996)
[4]  
Ilyas M., Straub J., Tomlinson I.P., Bodmer W.F., Genetic pathways in colorectal and other cancers, Eur. J. Cancer, 35, pp. 1986-2002, (1999)
[5]  
Smith G., Carey F.A., Beattie J., Wilkie M.J., Lightfoot T.J., Coxhead J., Garner R.C., Steele R.J., Wolf C.R., Mutations in APC, Kirsten-ras, and p53 - Alternative genetic pathways to colorectal cancer, Proc. Natl. Acad. Sci. USA, 99, pp. 9433-9438, (2002)
[6]  
Goss K.H., Groden J., Biology of the adenomatous polyposis coli tumor suppressor, J. Clin. Oncol., 18, pp. 1967-1979, (2000)
[7]  
Fearnhead N.S., Britton M.P., Bodmer W.F., The ABC of APC, Hum. Mol. Genet., 10, pp. 721-733, (2001)
[8]  
Hamilton S.R., Liu B., Parsons R.E., Papadopoulos N., Jen J., Powell S.M., Krush A.J., Berk T., Cohen Z., Tetu B., Burger P.C., Wood P.A., Taqi F., Booker S.V., Petersen G.M., Offerhaus G.J.A., Tersmette A.C., Giardiello F.M., Vogelstein B., Kinzler K.W., The molecular basis of Turcot's syndrome, N. Engl. J. Med., 332, pp. 839-847, (1995)
[9]  
Mediros A.C., Nagai M.A., Neto M.M., Brentani R.R., Loss of heterozygosity affecting the APC and MCC genetic loci in patients with primary breast carcinomas, Cancer Epidemiol. Biomarmers Prev., 3, pp. 331-333, (1994)
[10]  
Furuuchi K., Tada M., Yamada H., Kataoka A., Furuuchi N., Hamada J., Takahashi M., Todo S., Moriuchi T., Somatic mutations of the APC gene in primary breast cancers, Am. J. Pathol., 156, pp. 1997-2005, (2000)