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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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Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles

TL;DR: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasionOf cancer cells into the bone marrow microenvironment to allow a more flexible way to model the space competition between the two cell species.
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Frequent discordance between ERG gene rearrangement and ERG protein expression in a rapid autopsy cohort of patients with lethal, metastatic, castration-resistant prostate cancer

TL;DR: This data suggests that ERG IHC may be less sensitive for ERG rearrangements in castration‐resistant prostate cancer (CRPC), so a cohort of rapid autopsy patients with lethal metastatic CRPC with high ERG protein expression was sought.
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Genetic Ablation of Metadherin Inhibits Autochthonous Prostate Cancer Progression and Metastasis

TL;DR: It is reported that MTDH is amplified frequently in human prostate cancers where its expression levels are tightly correlated with prostate cancer progression and poor disease-free survival, and direct silencing of Mtdh in prostate cancer cells decreased proliferation in vitro and tumor growth in vivo, supporting an epithelial cell-intrinsic role of MTDH in prostatecancer.
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Phase II trial of oral cyclophosphamide, prednisone, and diethylstilbestrol for androgen-independent prostate carcinoma.

TL;DR: The authors evaluated the combination of oral cyclophosphamide, oral prednisone, and diethylstilbestrol in patients with androgen‐independent prostate carcinoma (AIPC).
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Wnt Signaling Drives Prostate Cancer Bone Metastatic Tropism and Invasion

TL;DR: A role for Wnt signaling as a driver of prostate cancer bone metastatic tropism and invasion is revealed and small molecule inhibition of JNK, which is an important component of the noncanonical WNT signaling pathway, significantly inhibited CM-mediated tumor invasion.