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Kenneth J. Pienta

Researcher at Johns Hopkins University School of Medicine

Publications -  751
Citations -  72579

Kenneth J. Pienta is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Prostate cancer & Cancer. The author has an hindex of 127, co-authored 671 publications receiving 64531 citations. Previous affiliations of Kenneth J. Pienta include Rutgers University & Harper University Hospital.

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Eleventh Prouts Neck Meeting on Prostate Cancer: Emerging Strategies in Prostate Cancer Therapy

TL;DR: The Prouts Neck Meetings on Prostate Cancer began in 1985 through the efforts of the Organ Systems Branch of the National Cancer Institute to stimulate new research and focused around specific questions in prostate tumorigenesis and therapy.
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The epidemiology of prostate cancer: clues for chemoprevention.

TL;DR: The ultimate goal of epidemiologic studies is to identify risk factors, i.e., promotional agents, for prostate cancer and to use this knowledge for disease prevention strategies.
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Enhanced invasion of hormone refractory prostate cancer cells through hepatocyte growth factor (HGF) induction of urokinase-type plasminogen activator (u-PA)

TL;DR: The biological significance of u-PA up-regulation in response to HGF in highly metastatic hormone refractory CaP cells is demonstrated, demonstrating the role of MET in contributing to prostate cancer metastasis.
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Novel molecular targets for prostate cancer therapy.

TL;DR: This review examines both laboratory and clinical advances using cell structure, growth factors, differentiating agents, angiogenesis, metastasis, and the cell cycle in the treatment of prostate cancer.
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Evidence for lectin signaling to the nuclear matrix: cellular interpretation of the glycocode

TL;DR: The cytoplasmic domains of integrins have been shown to bind to essential cytoskeletal proteins such as talin and a-actinin, and activate focal adhesion kinase in creating adhesion complexes, demonstrating an ability to bridge the gap between mechanical adhesion and intracellular signaling.