Molecular models for the tissue specificity of DNA mismatch repair-deficient carcinogenesis Review uri icon

Overview

MeSH Major

  • DNA Repair
  • Genetic Predisposition to Disease
  • Neoplasms

abstract

  • A common feature of all the known cancer genetic syndromes is that they predispose only to selective types of malignancy. However, many of the genes mutated in these syndromes are ubiquitously expressed, and influence seemingly universal processes such as DNA repair or cell cycle control. The tissue specificity of cancers that arise from malfunction of these apparently universal traits remains a key puzzle in cancer genetics. Mutations in DNA mismatch repair (MMR) genes cause the most common known cancer genetic syndrome, hereditary non-polyposis colorectal cancer, and the fundamental biology of MMR is one of the most intensively studied processes in laboratories all around the world. This review uses MMR as a model system to understand mechanisms that may explain the selective development of tumors in particular cell types despite the universal nature of this process. We evaluate recent data giving insights into the specific tumor types that are attributable to defective MMR in humans and mice under different modes of inheritance, and propose models that may explain the spectrum of cancer types observed.

publication date

  • March 20, 2006

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC1361617

Digital Object Identifier (DOI)

  • 10.1093/nar/gkj489

PubMed ID

  • 16464822

Additional Document Info

start page

  • 840

end page

  • 52

volume

  • 34

number

  • 3