Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer
Article Abstract:
Msh2 lacking cells have forfeited mismatch binding and gained microsatelite instability, a mutator phenotype and resistance to methylating agents. Homologous recombination has also given up reliance on absolute identity between interacting DNA sequences, indicating that Msh2 participates in saving the genome from promiscuous recombination. Msh2-lacking mice exhibit no big abnormalities in the preliminary phase. Hence Msh2 participates in DNA mismatch repair.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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Cross-species oncogenomics in cancer gene identification
Article Abstract:
The complexity of genomic aberrations in most human tumors has hampered the delineation of the genes that drive the tumorigenic process, but cognate mouse tumor models have recapitulated these genetic alterations with unexpected fidelity. The results have shown that cross-species genomic analysis can be used to identify the responsible genes and evaluate their oncogenic capacity in the appropriate genetic context.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2006
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Stem cells for lung cancer?
Article Abstract:
Researchers describe a niche in the bronchioalveolar duct junction of adult mouse lung that harbors stem cells from which adenocarcinomas are likely to arise. The new work offers perspectives on possible therapeutic interventions to combat lung cancer.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2005
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