PMID:7550317

Citation	Reitmair, AH, Schmits, R, Ewel, A, Bapat, B, Redston, M, Mitri, A, Waterhouse, P, Mittrücker, HW, Wakeham, A and Liu, B (1995) MSH2 deficient mice are viable and susceptible to lymphoid tumours. Nat. Genet. 11:64-70
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.
Links	PubMed Online version:10.1038/ng0995-64
Keywords	Animals; Base Sequence; Cell Transformation, Neoplastic/genetics; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics; DNA Repair/genetics; DNA, Neoplasm/analysis; DNA, Neoplasm/genetics; DNA, Satellite/analysis; DNA-Binding Proteins/genetics; Female; Fungal Proteins; Gene Targeting; Genotype; Humans; Lymphoid Tissue/pathology; Male; Meiosis; Mice; Mice, Knockout; Mice, Mutant Strains; Molecular Sequence Data; MutS Homolog 2 Protein; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology; Species Specificity
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