| Literature DB >> 17418409 |
Rong Wu1, Neali Hendrix-Lucas, Rork Kuick, Yali Zhai, Donald R Schwartz, Aytekin Akyol, Samir Hanash, David E Misek, Hidetaka Katabuchi, Bart O Williams, Eric R Fearon, Kathleen R Cho.
Abstract
One histologic subtype of ovarian carcinoma, ovarian endometrioid adenocarcinoma (OEA), frequently harbors mutations that constitutively activate Wnt/beta-catenin-dependent signaling. We now show that defects in the PI3K/Pten and Wnt/beta-catenin signaling pathways often occur together in a subset of human OEAs, suggesting their cooperation during OEA pathogenesis. Deregulation of these two pathways in the murine ovarian surface epithelium by conditional inactivation of the Pten and Apc tumor suppressor genes results in the formation of adenocarcinomas morphologically similar to human OEAs with 100% penetrance, short latency, and rapid progression to metastatic disease in upwards of 75% of mice. The biological behavior and gene expression patterns of the murine cancers resemble those of human OEAs with defects in the Wnt/beta-catenin and PI3K/Pten pathways.Entities:
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Year: 2007 PMID: 17418409 DOI: 10.1016/j.ccr.2007.02.016
Source DB: PubMed Journal: Cancer Cell ISSN: 1535-6108 Impact factor: 31.743