Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Colon Cancer Carcinogenesis in Human and in Experimental Animal Models

  • Takuji Tanaka
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_6520-2


Colon cancer (often subsumed under the term colorectal cancer (CRC), Fig. 1) develops as a result of the pathologic transformation of normal colonic epithelium to an adenomatous polyp and ultimately an invasive cancer. The multistep development requires years and possibly decades and is accompanied by a number of genetic alterations.


Ulcerative Colitis Familial Adenomatous Polyposis Lynch Syndrome Colonic Carcinogen Colitic Cancer 
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.
This is a preview of subscription content, log in to check access.


  1. Rosenberg DW, Giardina C, Tanaka T (2009) Mouse models for the study of colon carcinogenesis. Carcinogenesis 30(2):183–196. Epub 26 Nov 2008. Review. PubMed PMID: 19037092; PubMed Central PMCID: PMC2639048CrossRefPubMedPubMedCentralGoogle Scholar
  2. Takahashi M, Wakabayashi K (2004) Gene mutations and altered gene expression in azoxymethane-induced colon carcinogenesis in rodents. Cancer Sci 95(6):475–80. Review. PubMedCrossRefPubMedGoogle Scholar
  3. Taketo MM, Edelmann W (2009) Mouse models of colon cancer. Gastroenterology 136(3):780–798. Review. PubMedCrossRefPubMedGoogle Scholar
  4. Tanaka T (2009) Colorectal carcinogenesis: review of human and experimental animal studies. J Carcinog 8:5. PubMedCrossRefPubMedPubMedCentralGoogle Scholar
  5. Tanaka T, Kohno H, Suzuki R, Yamada Y, Sugie S, Mori H (2003) A novel inflammation-related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate. Cancer Sci 94(11):965–73. PubMedCrossRefPubMedGoogle Scholar
  6. Yasui Y, Kim M, Oyama T, Tanaka T (2009) Colorectal carcinogenesis and suppression of tumor development by inhibition of enzymes and molecular targets. Curr Enzyme Inhib 5:1–26CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Department of Oncologic PathologyKanazawa Medical UniversityKanazawaJapan