| First Author | Reitmair AH | Year | 1995 |
| Journal | Nat Genet | Volume | 11 |
| Issue | 1 | Pages | 64-70 |
| PubMed ID | 7550317 | Mgi Jnum | J:28397 |
| Mgi Id | MGI:76015 | Doi | 10.1038/ng0995-64 |
| Citation | Reitmair AH, et al. (1995) MSH2 deficient mice are viable and susceptible to lymphoid tumours. Nat Genet 11(1):64-70 |
| abstractText | 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. |
