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Article: MSH2 deficient mice are viable and susceptible to lymphoid tumours

TitleMSH2 deficient mice are viable and susceptible to lymphoid tumours
Authors
Issue Date1995
Citation
Nature Genetics, 1995, v. 11, n. 1, p. 64-70 How to Cite?
AbstractAlterations 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. © 1995 Nature Publishing Group.
Persistent Identifierhttp://hdl.handle.net/10722/292474
ISSN
2023 Impact Factor: 31.7
2023 SCImago Journal Rankings: 17.300
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorReitmair, A. H.-
dc.contributor.authorSchmits, R.-
dc.contributor.authorEwel, A.-
dc.contributor.authorBapat, B.-
dc.contributor.authorRedston, M.-
dc.contributor.authorMitri, A.-
dc.contributor.authorWaterhouse, P.-
dc.contributor.authorMittrücker, H. W.-
dc.contributor.authorWakeham, A.-
dc.contributor.authorLiu, B.-
dc.contributor.authorThomason, A.-
dc.contributor.authorGriesser, H.-
dc.contributor.authorGallinger, S.-
dc.contributor.authorBallhausen, W. G.-
dc.contributor.authorFishel, R.-
dc.contributor.authorMak, T. W.-
dc.date.accessioned2020-11-17T14:56:33Z-
dc.date.available2020-11-17T14:56:33Z-
dc.date.issued1995-
dc.identifier.citationNature Genetics, 1995, v. 11, n. 1, p. 64-70-
dc.identifier.issn1061-4036-
dc.identifier.urihttp://hdl.handle.net/10722/292474-
dc.description.abstractAlterations 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. © 1995 Nature Publishing Group.-
dc.languageeng-
dc.relation.ispartofNature Genetics-
dc.titleMSH2 deficient mice are viable and susceptible to lymphoid tumours-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/ng0995-64-
dc.identifier.pmid7550317-
dc.identifier.scopuseid_2-s2.0-0029111463-
dc.identifier.volume11-
dc.identifier.issue1-
dc.identifier.spage64-
dc.identifier.epage70-
dc.identifier.eissn1546-1718-
dc.identifier.isiWOS:A1995RR72800017-
dc.identifier.issnl1061-4036-

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