Alireza Heravi-Moussavi.

We conclude that in a variety of nonepithelial ovarian cancers, and other cancers potentially, aberrant miRNA processing resulting from DICER1 hot-spot mutations is a key oncogenic event.. Alireza Heravi-Moussavi, Ph.D., Michael S. Anglesio, Ph.D., S.-W. Grace Cheng, Ph.D., Janine Senz, B.Sc., Winnie Yang, B.Sc., Leah Prentice, Ph.D., Anthony P. Fejes, M.Sc., Christine Chow, B.M.L.Sc., Alicia Tone, Ph.D., Steve E. Kalloger, B.Sc., Nancy Hamel, M.Sc., Andrew Roth, B.Sc., Gavin Ha, B.Sc., Adrian N.C. Wan, B.Sc., Sarah Maines-Bandiera, M.Sc., Clara Salamanca, B.Sc., Barbara Pasini, M.D., Blaise A. Clarke, M.D., Anna F. Lee, M.D., Ph.D., Cheng-Han Lee, M.D., Ph.D., Chengquan Zhao, M.D., Robert H. Small, M.D., Samuel A. Aparicio, B.M., B.Ch., Ph.D., Poul H.B.Study participants had similar responses to therapy irrespective of their AR-V7 position. PSA responses were achieved in 41 % of AR-V7-positive males and in 65 % of AR-V7-negative males . This 41 % PSA response rate to taxane therapy is usually notable because the PSA response rate to abiraterone or enzalutamide in AR-V7-positive individuals was 0 % in the authors' prior study. The median progression-free survival to taxane therapy was comparable in AR-V7-positive and AR-V7-adverse men . The AR-V7 abnormality occurs more among patients who have undergone multiple lines of hormone therapies frequently. Scientists think that the AR-V7 abnormality is certainly triggered by chronic low testosterone levels and may become an adaptive response of the cancers to maintain AR signaling when the normal AR is inhibited.

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