| Literature DB >> 24491407 |
Hirohiko Yasui1, Norifumi Naka2, Yoshinori Imura3, Hidetatsu Outani3, Keiko Kaneko3, Ken-Ichiro Hamada3, Satoru Sasagawa4, Nobuhito Araki5, Takafumi Ueda6, Kazuyuki Itoh4, Akira Myoui3, Hideki Yoshikawa3.
Abstract
We examined efficacy of the mTOR inhibitor RAD001 to seek novel therapies for synovial sarcoma (SS). Although RAD001 had significant anti-tumor effects, its sensitivity differed among cell lines. Phospho-receptor tyrosine kinase (RTK) array analyses revealed c-MET phosphorylation in highly mTOR inhibitor-sensitive cells and PDGFRα (which induces intrinsic resistance to mTOR inhibitor) activation in less sensitive cells. Combined treatment with RAD001 and the PDGFR inhibitor pazopanib showed anti-tumor effects in xenograft models with less sensitive cells. Thus, evaluating activated RTKs in clinical samples may predict sensitivity to mTOR inhibitors, raising the possibility of a tailored therapy for SS.Entities:
Keywords: PDGFRα; RAD001; Receptor tyrosine kinase array; Synovial sarcoma; c-MET
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Year: 2014 PMID: 24491407 DOI: 10.1016/j.canlet.2014.01.027
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679