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Nat Genet. 1995 Sep;11(1):64-70.

MSH2 deficient mice are viable and susceptible to lymphoid tumours.

Author information

1
Amgen Institute, Department of Medical Biophysics, University of Toronto, Canada.

Abstract

Alterations of the human MSH2 gene, a homologue of the bacterial MutS mismatch repair gene, co-segregate with the majority of hereditary non-polyposis colon cancer (HNPCC) cases. We have generated homozygous MSH2-/- mice. Surprisingly, these mice were found to be viable, produced offspring in a mendelian ratio and bred through at least two generations. Starting at two months of age homozygous-/- mice began, with high frequency, to develop lymphoid tumours that contained microsatellite instabilities. These data establish a direct link between MSH2 deficiency and the pathogenesis of cancer. These mutant mice should be good models to study the progression of tumours and also to screen carcinogenic and anti-cancer agents.

PMID:
7550317
DOI:
10.1038/ng0995-64
[Indexed for MEDLINE]

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