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- W2316332924 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLNeuroblastoma, a tumor of peripheral neural crest origin, numbers among the most common childhood cancers. Both amplification of the proto-oncogene MYCN and increased vascular density mark high-risk disease. Since angiogenesis is regulated by phosphatidylinositol-3’ kinase (PI3K), we tested a clinical PI3K inhibitor, NVP-BEZ235, in MYCN-dependent neuroblastoma. NVP-BEZ235 decreased angiogenesis in a primary human neuroblastoma (MYCN-amplified orthotopic xenograft), and improved survival in a transgenic mouse model for MYCN-driven neuroblastoma. Using both gain and loss of function approaches, we demonstrate that the anti-angiogenic efficacy of NVP-BEZ235 was critically dependent on Mycn, in vitro and in-vivo. Thus, clinical PI3K/mTOR inhibitors drive degradation of Mycn in tumor cells, with secondary paracrine blockade of tumor-vascular microenvironment. These observations argue that NVP-BEZ235 should be tested in children with high-risk, MYCN amplified neuroblastoma.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1558. doi:10.1158/1538-7445.AM2011-1558" @default.
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- W2316332924 date "2011-04-15" @default.
- W2316332924 modified "2023-09-25" @default.
- W2316332924 title "Abstract 1558: Paracrine signaling through Mycn enhances tumor-vascular microenvironment in neuroblastoma" @default.
- W2316332924 doi "https://doi.org/10.1158/1538-7445.am2011-1558" @default.
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