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题目:: Combination therapy targeting both tumor-initiating and differentiated cell populations in prostate carcinoma.
作者:: Dubrovska(Anna),Elliott(Jimmy),Salamone(Richard J),Kim(Sungeun),Aimone(Lindsey J),Walker(John R),Watson(James),Sauveur-Michel(Maira),Garcia-Echeverria(Carlos),Cho(Charles Y),Reddy(Venkateshwar A),Schultz(Peter G)
状态:: 发布时间2010-12-08 , 更新时间 2016-11-25
期刊:: Clin Cancer Res
摘要:: The cancer stem cell hypothesis predicts that standard prostate cancer monotherapy eliminates bulk tumor cells but not a tumor-initiating cell population, eventually leading to relapse. Many studies have sought to determine the underlying differences between bulk tumor and cancer stem cells.,Our previous data suggest that the PTEN/PI3K/AKT pathway is critical for the in vitro maintenance of CD133(+)/CD44(+) prostate cancer progenitors and, consequently, that targeting PI3K signaling may be beneficial in treatment of prostate cancer.,Here, we show that inhibition of PI3K activity by the dual PI3K/mTOR inhibitor NVP-BEZ235 leads to a decrease in the population of CD133(+)/CD44(+) prostate cancer progenitor cells in vivo. Moreover, the combination of the PI3K/mTOR modulator NVP-BEZ235, which eliminates prostate cancer progenitor populations, and the chemotherapeutic drug Taxotere, which targets the bulk tumor, is significantly more effective in eradicating tumors in a prostate cancer xenograft model than monotherapy.,This combination treatment ultimately leads to the expansion of cancer progenitors with a PTEN E91D mutation, suggesting that the analysis of PTEN mutations could predict therapeutic response to the dual therapy.
语言:: eng
DOI:: 10.1158/1078-0432.CCR-10-1601

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