MSH2 deficient mice are viable and susceptible to lymphoid tumours

Nat Genet. 1995 Sep;11(1):64-70. doi: 10.1038/ng0995-64.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 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


  • DNA, Neoplasm
  • DNA, Satellite
  • DNA-Binding Proteins
  • Fungal Proteins
  • MutS Homolog 2 Protein