Journal
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Volume 17, Issue 1, Pages 17-26Publisher
WILEY
DOI: 10.1046/j.1440-1746.2002.02635.x
Keywords
adenoma; cancer; classification; colon; genetic instability; hereditary non-polyposis colorectal cancer; hyperplastic polyp
Categories
Ask authors/readers for more resources
This review compiles evidence for an alternative to the classical adenoma-carcinoma sequence in the evolution of colorectal cancer. It is suggested that between 30 and 50% of colorectal cancers are not initiated by mutation of the tumor suppressor gene APC, but through the epigenetic silencing of genes implicated in the control of differentiation, cell cycle control and DNA repair proficiency. The precursor polyps are often characterized by a serrated architecture, and include hyperplastic polyps, admixed polyps and serrated adenomas. The alternative pathway is heterogeneous and may culminate in cancers showing low or high level DNA microsatellite instability (MSI-L and MSI-H, respectively), and in cancers that are microsatellite stable (MSS). Cancers showing DNA MSI may be characterized by an accelerated evolution. Cancers in hereditary non-polyposis colorectal cancer show features of both classical (adenoma and APC mutation) and alternative pathways (rapid evolution, MSI-H and lack of chromosomal instability). (C) 2001 Blackwell Science Asia Pty Ltd.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available