K
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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RETRACTED: Different docetaxel-induced apoptotic pathways are present in prostate cancer cell lines LNCaP and PC-3
TL;DR: Two distinctly different Taxotere-induced apoptotic pathways in LNCaP and PC-3 cells that may be of clinical importance when treating prostate cancer are demonstrated.
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Prostate cancer research: The next generation; report from the 2019 Coffey-Holden Prostate Cancer Academy Meeting.
Andrea K. Miyahira,Adam Sharp,Adam Sharp,Leigh Ellis,Leigh Ellis,Leigh Ellis,Jennifer Jones,Salma Kaochar,H. Benjamin Larman,David A. Quigley,Huihui Ye,Jonathan W. Simons,Kenneth J. Pienta,Howard R. Soule +13 more
TL;DR: The 2019 Coffey‐Holden Prostate Cancer Academy (CHPCA) Meeting, “Prostate Cancer Research: The Next Generation,” was held 20 to 23 June, 2019, in Los Angeles, California.
Journal Article
Cell motility as a chemotherapeutic target.
TL;DR: Viewing the cell as a chemomechanical engine that relies on a tension based system for movement allows us to design chemotherapeutic strategies to inhibit tumour cell motility directly.
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Inhibition of prostate cancer growth by estramustine and colchicine
TL;DR: In clinically achievable concentrations, the combination of estramustine and colchicine was cytotoxic to both the Dunning rat prostate adenocarcinoma cell line MAT‐LyLu (MLL) and human prostate cancer cells (PC‐3).
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Prostate cancer promotes CD11b positive cells to differentiate into osteoclasts
TL;DR: It is demonstrated that functional osteoclasts can be derived from CD11b+ cells derived from human PBMCs, suggesting a potential RANKL‐independent mechanism of functional osteoclast formation.