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Mouse models for colorectal cancer.
Oncogene. 1999 Sep 20; 18(38):5325-33.O

Abstract

Colorectal cancer (CRC) is one of the most common cancers in the Western world. Much has been learned about colorectal cancer from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). Mouse models for CRC were generated by introducing mutations into the mouse genes, whose human counterparts were implicated in the onset and progression of CRC. Central among these are mice carrying mutations in the Adenomatous polyposis coli (Apc) gene. Although most of these Apc mutations share some common phenotypes as homozygous embryonic lethality and tumor predisposition, the severity of the tumor predisposition is variable. Mice with mutations in the mismatch repair genes, Msh2 and Mlh1, exhibit a mismatch repair defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other organ systems. Mice carrying a mutation in the Pms2 gene are predisposed to lymphomas and other tumors. Mice with a mutation in the Msh6 gene have a defect in base mismatch repair and show a tumor predisposition phenotype. Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis.

Authors+Show Affiliations

Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

10498885

Citation

Heyer, J, et al. "Mouse Models for Colorectal Cancer." Oncogene, vol. 18, no. 38, 1999, pp. 5325-33.
Heyer J, Yang K, Lipkin M, et al. Mouse models for colorectal cancer. Oncogene. 1999;18(38):5325-33.
Heyer, J., Yang, K., Lipkin, M., Edelmann, W., & Kucherlapati, R. (1999). Mouse models for colorectal cancer. Oncogene, 18(38), 5325-33.
Heyer J, et al. Mouse Models for Colorectal Cancer. Oncogene. 1999 Sep 20;18(38):5325-33. PubMed PMID: 10498885.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mouse models for colorectal cancer. AU - Heyer,J, AU - Yang,K, AU - Lipkin,M, AU - Edelmann,W, AU - Kucherlapati,R, PY - 1999/9/28/pubmed PY - 1999/9/28/medline PY - 1999/9/28/entrez SP - 5325 EP - 33 JF - Oncogene JO - Oncogene VL - 18 IS - 38 N2 - Colorectal cancer (CRC) is one of the most common cancers in the Western world. Much has been learned about colorectal cancer from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). Mouse models for CRC were generated by introducing mutations into the mouse genes, whose human counterparts were implicated in the onset and progression of CRC. Central among these are mice carrying mutations in the Adenomatous polyposis coli (Apc) gene. Although most of these Apc mutations share some common phenotypes as homozygous embryonic lethality and tumor predisposition, the severity of the tumor predisposition is variable. Mice with mutations in the mismatch repair genes, Msh2 and Mlh1, exhibit a mismatch repair defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other organ systems. Mice carrying a mutation in the Pms2 gene are predisposed to lymphomas and other tumors. Mice with a mutation in the Msh6 gene have a defect in base mismatch repair and show a tumor predisposition phenotype. Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/10498885/Mouse_models_for_colorectal_cancer_ L2 - http://dx.doi.org/10.1038/sj.onc.1203036 DB - PRIME DP - Unbound Medicine ER -