Advertisement

Colon Cancer

  • Dennis W. Ross
Chapter
  • 94 Downloads

Abstract

Colon cancer has a well defined, multistep evolution defined both by histology and by molecular events. Colon cancer occurs both in an hereditary pattern secondary to germline mutations and, more commonly, in a sporadic pattern secondary to somatic mutations. The molecular lesions of colon cancer appear years before invasive cancer. The cells lining the colon are bathed in a lifelong effluent of bacteria and breakdown products of digestion. Our knowledge of carcinogenesis agrees with epidemiologic evidence that suggests a high-fiber, lower-fat diet would decrease the incidence of colon cancer. Inert fiber moves stool through the colon faster, decreasing exposure of the lining cells to carcinogens. Less fat and more antioxidants in our diets may further shift the rate of carcinogenesis. (Recall the steps in Figure 5.2.)

Keywords

Colon Cancer Germline Mutation Familial Adenomatous Polyposis Colon Polyp Villous Adenoma 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Bischoff JR, Kim DH, Williams A, Heise C, Hom S, Muna M, Ng L, Hye JA, Sampson- Johannes A, Fattaey A, McCormick F. An adenovirus mutant that replicates selectively in p53-deficient human tumor cells. Science. 1996; 274:373–376.PubMedCrossRefGoogle Scholar
  2. Giardiello FM, Brensinger JD, Peterson GM, et al. The use and interpretation of commercial APC gene testing for familial adenomatous polyposis. New Engl J Med. 1997;336:823–827.PubMedCrossRefGoogle Scholar
  3. Laken SJ, Petersen GM, Gruber SB, et al. Familial colorectal cancer in Ashkenazim due to a hypermutable tract in APC. Nature Genetics. 1997; 17:79–83.PubMedCrossRefGoogle Scholar
  4. Tomlinson I, Ilyas M, Novelli M. Molecular genetics of colon cancer. Cancer and Metastasis Rev. 1997;16:67–79.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • Dennis W. Ross
    • 1
  1. 1.Department of PathologyForsyth Medical CenterWinston-SalemUSA

Personalised recommendations