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C-Myc Is a Critical Mediator of the Phenotypes of Apc Loss in the Intestine

C-Myc Is a Critical Mediator of the Phenotypes of Apc Loss in the Intestine The Adenomatous polyposis coli ( Apc ) gene is mutated in up to 80% of sporadic colorectal cancers. After Apc loss, there is deregulation of the Wnt signaling pathway and transactivation of T-cell factor/leukemia enhancing factor target genes such as C-Myc . This review focuses on recent data highlighting the importance of the C-Myc oncogene and its transcriptional targets in establishing all of the phenotypes caused by the deletion of the Apc tumor suppressor gene within the intestinal epithelium. The importance of investigating Apc and C-Myc gene function in the correct tissue context is also discussed. Cancer Res 2008;68(13):4963–6 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cancer Research American Association of Cancer Research

C-Myc Is a Critical Mediator of the Phenotypes of Apc Loss in the Intestine

Cancer Research , Volume 68 (13): 4963 – Jul 1, 2008

C-Myc Is a Critical Mediator of the Phenotypes of Apc Loss in the Intestine

Cancer Research , Volume 68 (13): 4963 – Jul 1, 2008

Abstract

The Adenomatous polyposis coli ( Apc ) gene is mutated in up to 80% of sporadic colorectal cancers. After Apc loss, there is deregulation of the Wnt signaling pathway and transactivation of T-cell factor/leukemia enhancing factor target genes such as C-Myc . This review focuses on recent data highlighting the importance of the C-Myc oncogene and its transcriptional targets in establishing all of the phenotypes caused by the deletion of the Apc tumor suppressor gene within the intestinal epithelium. The importance of investigating Apc and C-Myc gene function in the correct tissue context is also discussed. Cancer Res 2008;68(13):4963–6

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References (32)

Publisher
American Association of Cancer Research
Copyright
Copyright © 2008 by the American Association for Cancer Research.
ISSN
0008-5472
DOI
10.1158/0008-5472.CAN-07-5558
pmid
18593890
Publisher site
See Article on Publisher Site

Abstract

The Adenomatous polyposis coli ( Apc ) gene is mutated in up to 80% of sporadic colorectal cancers. After Apc loss, there is deregulation of the Wnt signaling pathway and transactivation of T-cell factor/leukemia enhancing factor target genes such as C-Myc . This review focuses on recent data highlighting the importance of the C-Myc oncogene and its transcriptional targets in establishing all of the phenotypes caused by the deletion of the Apc tumor suppressor gene within the intestinal epithelium. The importance of investigating Apc and C-Myc gene function in the correct tissue context is also discussed. Cancer Res 2008;68(13):4963–6

Journal

Cancer ResearchAmerican Association of Cancer Research

Published: Jul 1, 2008

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