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Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer.
Am J Med Genet C Semin Med Genet. 2004 Aug 15; 129C(1):91-9.AJ

Abstract

Germline mutations in DNA mismatch repair genes underlie one of the most common hereditary cancer predisposition syndromes known in humans, hereditary nonpolyposis colorectal cancer (HNPCC). Defects of the DNA mismatch repair system are also prevalent in sporadic colorectal cancers. The generation of mice with targeted inactivating mutations in the mismatch repair genes has facilitated the in vivo study of how these genes function and how their individual loss contributes to tumorigenesis. Although there are notable limitations when using murine models to study the molecular basis of human cancer, there is remarkable similarity between the two species with respect to the contribution of individual members of the mismatch repair system to cancer susceptibility, and mouse mutants have greatly enhanced our understanding of the normal role of these genes in mutation avoidance and suppression of tumorigenesis.

Authors+Show Affiliations

Human Genetics, Mt. Sinai School of Medicine, New York, NY, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

15264277

Citation

Edelmann, Lisa, and Winfried Edelmann. "Loss of DNA Mismatch Repair Function and Cancer Predisposition in the Mouse: Animal Models for Human Hereditary Nonpolyposis Colorectal Cancer." American Journal of Medical Genetics. Part C, Seminars in Medical Genetics, vol. 129C, no. 1, 2004, pp. 91-9.
Edelmann L, Edelmann W. Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer. Am J Med Genet C Semin Med Genet. 2004;129C(1):91-9.
Edelmann, L., & Edelmann, W. (2004). Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer. American Journal of Medical Genetics. Part C, Seminars in Medical Genetics, 129C(1), 91-9.
Edelmann L, Edelmann W. Loss of DNA Mismatch Repair Function and Cancer Predisposition in the Mouse: Animal Models for Human Hereditary Nonpolyposis Colorectal Cancer. Am J Med Genet C Semin Med Genet. 2004 Aug 15;129C(1):91-9. PubMed PMID: 15264277.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Loss of DNA mismatch repair function and cancer predisposition in the mouse: animal models for human hereditary nonpolyposis colorectal cancer. AU - Edelmann,Lisa, AU - Edelmann,Winfried, PY - 2004/7/21/pubmed PY - 2004/9/24/medline PY - 2004/7/21/entrez SP - 91 EP - 9 JF - American journal of medical genetics. Part C, Seminars in medical genetics JO - Am J Med Genet C Semin Med Genet VL - 129C IS - 1 N2 - Germline mutations in DNA mismatch repair genes underlie one of the most common hereditary cancer predisposition syndromes known in humans, hereditary nonpolyposis colorectal cancer (HNPCC). Defects of the DNA mismatch repair system are also prevalent in sporadic colorectal cancers. The generation of mice with targeted inactivating mutations in the mismatch repair genes has facilitated the in vivo study of how these genes function and how their individual loss contributes to tumorigenesis. Although there are notable limitations when using murine models to study the molecular basis of human cancer, there is remarkable similarity between the two species with respect to the contribution of individual members of the mismatch repair system to cancer susceptibility, and mouse mutants have greatly enhanced our understanding of the normal role of these genes in mutation avoidance and suppression of tumorigenesis. SN - 1552-4868 UR - https://www.unboundmedicine.com/medline/citation/15264277/Loss_of_DNA_mismatch_repair_function_and_cancer_predisposition_in_the_mouse:_animal_models_for_human_hereditary_nonpolyposis_colorectal_cancer_ L2 - https://doi.org/10.1002/ajmg.c.30021 DB - PRIME DP - Unbound Medicine ER -