The utility of Apc-mutant rats in modeling human colon cancer
Prior to the advent of genetic engineering in the mouse, the rat was the model of choice for investigating the etiology of cancer. Now, recent advances in the manipulation of the rat genome, combined with a growing recognition of the physiological differences between mice and rats, have reignited in...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
The Company of Biologists
2014-11-01
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| Series: | Disease Models & Mechanisms |
| Subjects: | |
| Online Access: | http://dmm.biologists.org/content/7/11/1215 |
| _version_ | 1819092162683338752 |
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| author | Amy A. Irving Kazuto Yoshimi Marcia L. Hart Taybor Parker Linda Clipson Madeline R. Ford Takashi Kuramoto William F. Dove James M. Amos-Landgraf |
| author_facet | Amy A. Irving Kazuto Yoshimi Marcia L. Hart Taybor Parker Linda Clipson Madeline R. Ford Takashi Kuramoto William F. Dove James M. Amos-Landgraf |
| author_sort | Amy A. Irving |
| collection | DOAJ |
| description | Prior to the advent of genetic engineering in the mouse, the rat was the model of choice for investigating the etiology of cancer. Now, recent advances in the manipulation of the rat genome, combined with a growing recognition of the physiological differences between mice and rats, have reignited interest in the rat as a model of human cancer. Two recently developed rat models, the polyposis in the rat colon (Pirc) and Kyoto Apc Delta (KAD) strains, each carry mutations in the intestinal-cancer-associated adenomatous polyposis coli (Apc) gene. In contrast to mouse models carrying Apc mutations, in which cancers develop mainly in the small intestine rather than in the colon and there is no gender bias, these rat models exhibit colonic predisposition and gender-specific susceptibility, as seen in human colon cancer. The rat also provides other experimental resources as a model organism that are not provided by the mouse: the structure of its chromosomes facilitates the analysis of genomic events, the size of its colon permits longitudinal analysis of tumor growth, and the size of biological samples from the animal facilitates multiplexed molecular analyses of the tumor and its host. Thus, the underlying biology and experimental resources of these rat models provide important avenues for investigation. We anticipate that advances in disease modeling in the rat will synergize with resources that are being developed in the mouse to provide a deeper understanding of human colon cancer. |
| first_indexed | 2024-12-21T22:51:14Z |
| format | Article |
| id | doaj.art-e627bb63238d47cfbb1f092913536550 |
| institution | Directory Open Access Journal |
| issn | 1754-8403 1754-8411 |
| language | English |
| last_indexed | 2024-12-21T22:51:14Z |
| publishDate | 2014-11-01 |
| publisher | The Company of Biologists |
| record_format | Article |
| series | Disease Models & Mechanisms |
| spelling | doaj.art-e627bb63238d47cfbb1f0929135365502022-12-21T18:47:35ZengThe Company of BiologistsDisease Models & Mechanisms1754-84031754-84112014-11-017111215122510.1242/dmm.016980016980The utility of Apc-mutant rats in modeling human colon cancerAmy A. IrvingKazuto YoshimiMarcia L. HartTaybor ParkerLinda ClipsonMadeline R. FordTakashi KuramotoWilliam F. DoveJames M. Amos-LandgrafPrior to the advent of genetic engineering in the mouse, the rat was the model of choice for investigating the etiology of cancer. Now, recent advances in the manipulation of the rat genome, combined with a growing recognition of the physiological differences between mice and rats, have reignited interest in the rat as a model of human cancer. Two recently developed rat models, the polyposis in the rat colon (Pirc) and Kyoto Apc Delta (KAD) strains, each carry mutations in the intestinal-cancer-associated adenomatous polyposis coli (Apc) gene. In contrast to mouse models carrying Apc mutations, in which cancers develop mainly in the small intestine rather than in the colon and there is no gender bias, these rat models exhibit colonic predisposition and gender-specific susceptibility, as seen in human colon cancer. The rat also provides other experimental resources as a model organism that are not provided by the mouse: the structure of its chromosomes facilitates the analysis of genomic events, the size of its colon permits longitudinal analysis of tumor growth, and the size of biological samples from the animal facilitates multiplexed molecular analyses of the tumor and its host. Thus, the underlying biology and experimental resources of these rat models provide important avenues for investigation. We anticipate that advances in disease modeling in the rat will synergize with resources that are being developed in the mouse to provide a deeper understanding of human colon cancer.http://dmm.biologists.org/content/7/11/1215APCAllelic seriesAnimal modelsColorectal cancer |
| spellingShingle | Amy A. Irving Kazuto Yoshimi Marcia L. Hart Taybor Parker Linda Clipson Madeline R. Ford Takashi Kuramoto William F. Dove James M. Amos-Landgraf The utility of Apc-mutant rats in modeling human colon cancer Disease Models & Mechanisms APC Allelic series Animal models Colorectal cancer |
| title | The utility of Apc-mutant rats in modeling human colon cancer |
| title_full | The utility of Apc-mutant rats in modeling human colon cancer |
| title_fullStr | The utility of Apc-mutant rats in modeling human colon cancer |
| title_full_unstemmed | The utility of Apc-mutant rats in modeling human colon cancer |
| title_short | The utility of Apc-mutant rats in modeling human colon cancer |
| title_sort | utility of apc mutant rats in modeling human colon cancer |
| topic | APC Allelic series Animal models Colorectal cancer |
| url | http://dmm.biologists.org/content/7/11/1215 |
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