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

JA Wilkins, OJ Sansom - Cancer research, 2008 - AACR
JA Wilkins, OJ Sansom
Cancer research, 2008AACR
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 …
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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