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10.1016/j.ccell.2016.03.001

http://scihub22266oqcxt.onion/10.1016/j.ccell.2016.03.001
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C4829466!4829466!27050099
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suck abstract from ncbi


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pmid27050099      Cancer+Cell 2016 ; 29 (4): 536-47
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  • N-Myc Drives Neuroendocrine Prostate Cancer Initiated from Human Prostate Epithelial Cells #MMPMID27050099
  • Lee JK; Phillips JW; Smith BA; Park JW; Stoyanova T; McCaffrey EF; Baertsch R; Sokolov A; Meyerowitz JG; Mathis C; Cheng D; Stuart JM; Shokat KM; Gustafson WC; Huang J; Witte ON
  • Cancer Cell 2016[Apr]; 29 (4): 536-47 PMID27050099show ga
  • MYCN amplification and overexpression are common in neuroendocrine prostate cancer (NEPC). However, the impact of aberrant N-Myc expression in prostate tumorigenesis and the cellular origin of NEPC have not been established. We define N-Myc and activated AKT1 as oncogenic components sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and NEPC with phenotypic and molecular features of aggressive, late-stage human disease. We directly show that prostate adenocarcinoma and NEPC can arise from a common epithelial clone. Further, N-Myc is required for tumor maintenance and destabilization of N-Myc through Aurora A kinase inhibition reduces tumor burden. Our findings establish N-Myc as a driver of NEPC and a target for therapeutic intervention.
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