Journal of Gastroenterology

, Volume 41, Issue 3, pp 185–192

Colorectal cancer: genetics of development and metastasis

Authors

  • Tetsuji Takayama
    • Fourth Department of Internal MedicineSapporo Medical University, School of Medicine
  • Koji Miyanishi
    • Fourth Department of Internal MedicineSapporo Medical University, School of Medicine
  • Tsuyoshi Hayashi
    • Fourth Department of Internal MedicineSapporo Medical University, School of Medicine
  • Yasushi Sato
    • Fourth Department of Internal MedicineSapporo Medical University, School of Medicine
  • Yoshiro Niitsu
    • Fourth Department of Internal MedicineSapporo Medical University, School of Medicine
Review

DOI: 10.1007/s00535-006-1801-6

Cite this article as:
Takayama, T., Miyanishi, K., Hayashi, T. et al. J Gastroenterol (2006) 41: 185. doi:10.1007/s00535-006-1801-6

Abstract

It has been well documented that there are two major pathways in colorectal carcinogenesis. One is the chromosomal instability pathway (adenoma–carcinoma sequence), which is characterized by allelic losses on chromosome 5q (APC), 17p (p53), and 18q (DCC/SMAD4), and the other is a pathway that involves microsatellite instability. Recent progress in molecular biology, however, has shown that colorectal carcinogenesis is not necessarily clearly divided into these two pathways, but is in fact more complicated. Other routes, including the transforming growth factor-β/SMAD pathway, the serrated pathway, and the epigenetic pathway, have been reported. Cross talk among these pathways has also been reported. In the invasion and metastasis steps of colorectal cancers, many more genes have now been identified as being involved in proteolysis, adhesion, angiogenesis, and cell growth. Recently accumulated evidence indicates that colorectal cancer is a genetically heterogeneous and complicated disease.

Key words

colorectal cancerchromosomal instabilitymicrosatellite instabilitymetastasis

Copyright information

© Springer-Verlag Tokyo 2006