作者: Hyeong-nam Jeong
DOI: 10.21236/ADA484145
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摘要: Abstract : Although Prostate cancer is the most common and second leading cause of cancer-related deaths in American men lack animal models that faithfully recapitulate histopathological clinical features human prostate has hampered research. Taking advantage a unique androgen-insensitive transgene promoter system we developed novel genetically-engineered mouse (GEM) model invasive adenocarcinoma whereby an activating mutation BRAFV600E been targeted to epithelial compartment gland. As first step for characterization this attempted assess requirement continuous BRAF*-ERK activation maintenance established lesions progression androgen-independent state. To our surprise found while sufficient initiate development AKT-independent not required its maintenance. In addition also demonstrated BRAF driven ERK S6K alone drive growth post castration although it appears be permissive survival low androgen