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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Book ChapterDOI
Targeting chemokine (C-C motif) ligand 2 (CCL2) as an example of translation of cancer molecular biology to the clinic.
TL;DR: In this chapter, targeting CCL2 in prostate cancer will be used as an example to show translation of laboratory findings from cancer molecular biology to the clinic.
Methylacyl Coenzyme A Racemase as a Tissue Biomarker for Prostate Cancer
Mark A. Rubin,Ming Zhou,Saravana M. Dhanasekaran,Sooryanarayana Varambally,Terrence R. Barrette,Martin G. Sanda,Kenneth J. Pienta,Debashis Ghosh,Arul M. Chinnaiyan +8 more
TL;DR: Development of additional serum and tissue biomarkers to supplement PSA screening is needed and molecular profiling establishes a new perspective in the study of cancer.
Journal ArticleDOI
Hematopoietic Stem Cell Niche Is a Potential Therapeutic Target for Bone Metastatic Tumors
TL;DR: Findings suggest that the bone marrow HSC niche is a potential therapeutic target for metastatic disease and the concept of targeting the niche in conjunction with chemotherapy could open up new possibilities to eradicate incurable metastatic diseases.
Journal Article
An in vitro and in vivo study of antitumor effects of genistein on hormone refractory prostate cancer.
TL;DR: Genistein appears to be cytotoxic to both the rat prostate cancer cell line MAT-LyLu and the human prostate adenocarcinoma cell line, PC-3, in vitro, and in vivo, however, genistein failed to significantly inhibit the growth of subcutaneously implanted MAT- LyLu cells.
Journal ArticleDOI
PAR1-mediated NFκB activation promotes survival of prostate cancer cells through a Bcl-xL-dependent mechanism
Kwanchanit Tantivejkul,Robert D. Loberg,Samkeliso Mawocha,LaShon L. Day,Lauren N. St. John,Brian A. Pienta,Mark A. Rubin,Kenneth J. Pienta +7 more
TL;DR: Because thrombin and PAR1 are over‐expressed in prostate cancer patients, targeting the inhibition of their interaction may attenuate NFκB signaling transduction resulting in decreased drug resistance and subsequent survival of prostate cancer cells.