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HOXB13 and other high penetrant genes for prostate cancer

Asian Journal of Andrology 2016年第4期18卷 530-532页

作者： patrick g pilie Veda N giri Kathleen A Cooney Division of Cancer Medicine The University of Texas MD Anderson Cancer Center Houston TX USA Department of Medical Oncology Sidney Kimmel Cancer Center Thomas Jefferson University Philadelphia PA USA Division of Hematology/ Oncology Department of Internal Medicine University of Michigan Medical School and The University of Michigan Comprehensive Cancer Center Ann Arbor MI USA

Cancer initiation and progression is the result of an accumulation of mutations inkey tumor suppressor genes, mismatch repair genes, or oncogenes, which impact cancer cell growth, death, and differentiation. Mutations occurring in cancer tissue are termed somatic; whereas, heritable mutatons that may be passed onto subsequent generations occur in germline DNA. It is these germline mutations that can lead to cancer family syndromeswhereby family members carrying a deleterious germline mutation have an increased susceptibility to certain cancer phenotypes. Common features of hereditary cancer syndromes include early age-of-onset, multiple affected generations, rare tumor types, and/or multiple primary malignancies.

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Fluoxetine induces cytotoxic endoplasmic reticulum stress and autophagy in triple negative breast cancer

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World Journal of Clinical Oncology 2015年第6期6卷 299-311页

作者： 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 Department of Medicine Division of Medical OncologyDuke University Medical Center Department of Internal Medicine University of Michigan Center for Applied Proteomics and Molecular Medicine George Mason University Department of Molecular and Cellular Oncology University of Texas MD Anderson Cancer Center

AIM: To investigate the mechanism of action of lipophilic antidepressant fluoxetine(FLX) in representative molecular subtypes of breast ***: 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 ***: 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.

关键词： Inflammatory breast cancer Endoplasmic reticulum stress Autophagy Apoptosis Fluoxetine

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