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6篇 您的检索式:作者名="Adrian Carter"
    题名 作者 年代 出处 被引量
1Phase I dose-escalation study of AZD7762, a checkpoint kinase inhibitor, in combination with gemcitabine in US patients with advanced solid tumors显示文摘Edward Sausville Patricia LoRusso Michael Carducci Judith Carter Mary F. Quinn Lisa Malburg Nilofer Azad David Cosgrove Richard Knight Peter Barker Sonya Zabludoff Felix Agbo Patricia Oakes Adrian Senderowicz 2014Cancer Chemotherapy and Pharmacology2014,,3:1
2Price reform and household demand for electricity显示文摘Adrian Carter Roland Craigwell Winston Moore 2011Journal of Policy Modeling2011,,2:1
3New technology advances applications for high-power fiber lasers显示文摘Adrian Carter Bryce Samson 2005Military & Aerospace Electronics2005,16,7:1
4New technology advances applications for high-power fiber lasers 显示文摘Adrian Carter Bryce Samson 2005Military Aerospace Electronics2005,16,7:1
5New technology advances applications for high-power fiber lasers显示文摘Adrian Carter Bryce Samson 2005MiIitary~ Aerospace Electronics2005,,7:1
6Fluoxetine induces cytotoxic endoplasmic reticulum stress and autophagy in triple negative breast cancer显示文摘AIM: To investigate the mechanism of action of lipophilic antidepressant fluoxetine(FLX) in representative molecular subtypes of breast cancer.METHODS: The anti-proliferative effects and mechanistic action of FLX in triple-negative(SUM149PT) and luminal(T47D and Au565) cancer cells and nontransformed MCF10 A were investigated. Reverse phase protein microarray(RPPM) was performed with and without 10 μmol/L FLX for 24 and 48 h to determine which proteins are significantly changed. Viability and cell cycle analysis were also performed to determine drug effects on cell growth. Western blotting was used to confirm the change in protein expression examined by RPPM or pursue other signaling proteins. RESULTS: The FLX-induced cell growth inhibition in all cell lines was concentration- and time-dependent but less pronounced in early passage MCF10 A. In comparison to the other lines,cell growth reduction in SUM149 PT coincided with significant induction of endoplasmic reticulum(ER) stress and autophagy after 24 and 48 h of 10 μmol/L FLX,resulting in decreased translation of proteins along the receptor tyrosine kinase/Akt/mammalian target of rapamycin pathways. The increase in autophagy marker,cleaved microtubule-associated protein 1 light chain 3,in SUM149 PT after 24 h of FLX was likely due to increased metabolic demands of rapidly dividing cells and ER stress. Consequently,the unfolded protein response mediated by double-stranded RNA-dependent protein kinase-like ER kinase resulted in inhibition of protein synthesis,growth arrest at the G1 phase,autophagy,and caspase-7-mediated cell death.CONCLUSION: Our study suggests a new role for FLX as an inducer of ER stress and autophagy,resulting in death of aggressive triple negative breast cancer SUM149 PT.Michelle Bowie Patrick Pilie Julia Wulfkuhle Siya Lem Abigail Hoffman Shraddha Desai Emanuel Petricoin Amira Carter Adrian Ambrose Victoria Seewaldt Dihua Yu Catherine Ibarra Drendall 2015World Journal of Clinical Oncology2015,6,6:1
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