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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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Identification of gene copy number and whole-genome methylation changes associated with lethal metastatic castration-resistant prostate cancer (CRPC).

TL;DR: This is the first known study examining both gene copy number and whole genome CpG island methylation status in metastatic CRPC, suggesting that inactivation of this tumor suppressor through multiple pathways is critical to tumor cell survival.
Proceedings ArticleDOI

Abstract 2229: CD133+/CD44+ Cancer Stem Cells Represent a Disproportionately Large Fraction of Early Bone Disseminated Prostate Cancer Tumor Cells

TL;DR: Early bone disseminated prostate cancer cells in murine xenograft models can be enriched by lineage depletion, identified by human leukocyte antigen, and subsequently isolated and characterized by flow cytometry, suggesting a proclivity for bone dissemination by CD133+/CD44+ prostate cancer stem cells and a possible role for these cells as DTCs responsible for biochemical failure after curative prostatectomy.
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Response to “Comment on ‘A method to measure cellular adhesion utilizing a polymer micro-cantilever’” [Appl. Phys. Lett. 104, 236103 (2014)]

TL;DR: This reply is in response to a Comment posed by Eibl on a paper to present a new adhesion measurement tool, and it is believed that meaningful results can be inferred by chemical cross-linking as explained below.
Journal Article

A novel orally active MDM2 inhibitor (MI-219) activates the p53 pathway and is selectively toxic to tumor cells

TL;DR: This study concludes that activation of p53 by potent and specific small-molecule MDM2 inhibitors is selectively toxic to tumors without causing damage to normal tissues, and provides a strong rationale to advance MI-219 or its analogues for clinical development as a new and promising cancer therapeutic strategy.
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Piflufolastat F-18 (18F-DCFPyL) for PSMA PET imaging in prostate cancer 

TL;DR: The remarkable diagnostic accuracy of PSMA-PET is reshaping prostate cancer imaging and the modularity of these agents hint at exciting new diagnostic and therapeutic opportunities that have the potential to improve the care of patients with prostate cancer as a whole.