Loss of DNA mismatch repair function and cancer predisposition in the mouse

Animal models for human hereditary nonpolyposis colorectal cancer

Lisa Edelmann, Winfried Edelmann

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

Germline mutations in DNA mismatch repair genes underlie one of the most common hereditary cancer predisposition syndromes known in humans, hereditary nonpolyposis colorectal cancer (HNPCC). Defects of the DNA mismatch repair system are also prevalent in sporadic colorectal cancers. The generation of mice with targeted inactivating mutations in the mismatch repair genes has facilitated the in vivo study of how these genes function and how their individual loss contributes to tumorigenesis. Although there are notable limitations when using murine models to study the molecular basis of human cancer, there is remarkable similarity between the two species with respect to the contribution of individual members of the mismatch repair system to cancer susceptibility, and mouse mutants have greatly enhanced our understanding of the normal role of these genes in mutation avoidance and suppression of tumorigenesis.

Original languageEnglish (US)
Pages (from-to)91-99
Number of pages9
JournalAmerican Journal of Medical Genetics - Seminars in Medical Genetics
Volume129 C
Issue number1
StatePublished - Aug 15 2004

Fingerprint

Hereditary Nonpolyposis Colorectal Neoplasms
DNA Mismatch Repair
Animal Models
Genes
Neoplasms
Carcinogenesis
Hereditary Neoplastic Syndromes
Mutation
Germ-Line Mutation
Colorectal Neoplasms

Keywords

  • DNA mismatch repair
  • HNPCC
  • Mouse models
  • Review

ASJC Scopus subject areas

  • Genetics(clinical)
  • Neuropsychology and Physiological Psychology
  • Neuroscience(all)

Cite this

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