• KOLs Community
    • Prostate
    • Prostate Cancer
    • Kenneth J Pienta
    • Kenneth J Pienta

      Kenneth J Pienta

      The James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA, jhu.edu | Cellular and Molecular ...



      KOL Resume for Kenneth J Pienta


      The James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA, jhu.edu

      Cellular and Molecular Medicine Program, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA;, (S.R.A.);, (K.J.P.)

      Johns Hopkins School of Medicine, Baltimore, MD,


      The Brady Urological Institute, Johns Hopkins School of Medicine, 600 N. Wolfe Street, Baltimore, MD 21287, USA

      Johns Hopkins School of Medicine, Cambridge, MA, United States


      The James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins University School of Medicine, 601 N. Caroline St., JHOC Room 3233, Baltimore, MD, USA

      Department of Medical Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland

      Johns Hopkins School of Medicine


      James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, 21205, Baltimore, MD, USA

      Department of Pharmacology and Molecular Sciences, The Johns Hopkins School of Medicine, Baltimore, Maryland

      Johns Hopkins Medical Institute.



      Kenneth J Pienta: Influence Statistics

      Sample of concepts for which Kenneth J Pienta is among the top experts in the world.
      Concept World rank
      psa levels prostatectomy #1
      vcap #1
      ttni dmfs #1
      genetic variation ccl2 #1
      interleukin4 map kinase #1
      pca p50imc #1
      cancer evolution factors #1
      global expression patterns #1
      sabr rsabr #1
      cellular growth survival #1
      detrusor myocytes cytoskeleton #1
      prostate cancer humans #1
      rpfs 95ci #1
      heritable variation conditions #1
      decline dkk1 #1
      proceduresbaseline #1
      pentosan mechanism #1
      srt docetaxel #1
      lds paccs #1
      absence bph #1
      hypoxia stabilizes #1
      twist1 chromatin #1
      dnmt1 emt #1
      pc3emt evs #1
      suvmean tlpsma #1
      detrusor mechanical stimulus #1
      protein macrophage polarization #1
      cancer cell paccs #1
      myeloid klf4 #1
      hoxa9 mouse prostate #1
      urology biochemical recurrence #1
      loss ndrg1 #1
      acellular analytes #1
      1532t #1
      arm 3 years #1
      adt onset #1
      dormancy regulator #1
      protein kinase dnmt1 #1
      estramustine oral #1
      laclleu tfag #1
      vibrational cell #1
      mtss1 mim #1
      fate separation #1
      chemotherapy aipc #1
      preclinical prostate #1
      complex drug landscape #1
      invasion invasive potential #1
      decrease psa #1
      sabrmethodsrecords #1
      sabr versus sabr #1


      Prominent publications by Kenneth J Pienta

      KOL-Index: 17882

      CONTEXT: Molecular profiling of prostate cancer has led to the identification of candidate biomarkers and regulatory genes. Discoveries from these genome-scale approaches may have applicability in the analysis of diagnostic prostate specimens.

      OBJECTIVES: To determine the expression and clinical utility of alpha-methylacyl coenzyme A racemase (AMACR), a gene identified as being overexpressed in prostate cancer by global profiling strategies.

      DESIGN: Four gene expression data sets from ...

      Known for Prostate Cancer | Tissue Biomarker | Messenger Racemases | Specificity Amacr | Tumor Biopsy
      KOL-Index: 16253

      Resistance to cell death is a hallmark of cancer. Autophagy is a survival mechanism activated in response to nutrient deprivation; however, excessive autophagy will ultimately induce cell death in a nonapoptotic manner. The present study demonstrates that CCL2 protects prostate cancer PC3 cells from autophagic death, allowing prolonged survival in serum-free conditions. Upon serum starvation, CCL2 induced survivin up-regulation in PC3, DU 145, and C4-2B prostate cancer cells. Both cell ...

      Known for Autophagic Death | Pc3 Cells | Phosphatidylinositol 3 | Prostate Cancer | Cell Survival
      KOL-Index: 15981

      It has been proposed that a 356 amino acid protein encoded by the MIM (Missing In Metastasis) gene on Chromosome 8q24.1, is a bladder cancer metastasis suppressor. Recently, Machesky and colleagues [Biochem. J. 371 (2003) 463] identified MIM-B, a 759 amino acid protein, of which the C-terminal 356 amino acids are almost identical to MIM. Importantly, PCR primers and Northern Blotting probes used in the studies of MIM in bladder cancer did not distinguish between sequences specific for ...

      Known for Cell Lines | Bladder Cancer | Metastasis Suppressor | Genetic Rna | Neoplasm Proteins
      KOL-Index: 15108

      Cancer metastasis is a multistep process associated with the induction of an epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs). Although significant progress has been made in understanding the molecular mechanisms regulating EMT and the CSC phenotype, little is known of how these processes are regulated by epigenetics. Here we demonstrate that reduced expression of DNA methyltransferase 1 (DNMT1) plays an important role in the induction of EMT and the CSC phenotype by ...

      Known for Cancer Metastasis | Stem Cells | Mesenchymal Transition | Emt Dnmt1 | Tumor Cell
      KOL-Index: 15066

      Antiapoptotic members of the Bcl-2 family proteins are overexpressed in prostate cancer and are promising molecular targets for modulating chemoresistance of prostate cancer. (-)-Gossypol, a natural BH3 mimetic, is a small-molecule inhibitor of Bcl-2/Bcl-xL/Mcl-1 currently in phase II clinical trials as an adjuvant therapy for human prostate cancer. Our objective is to examine the chemosensitization potential of (-)-gossypol in prostate cancer and its molecular mechanisms of action. ...

      Known for Prostate Cancer | Natural Bh3 Mimetic | Bcl2 Proteins | Antitumor Activity | Noxa Puma
      KOL-Index: 14890

      At autopsy >or=80% of prostate cancers have established macrometastases in marrow containing bone. The mechanism(s) to explain this remarkable level of bone involvement remain to be elucidated. We examined the adhesive and invasive behavior of prostate cancer cells to osteoblastic and human bone marrow endothelial cells (HBME-1) in an attempt to explain the tropism of prostate cells for bone. We found an inverse relationship between adhesion and prostate cell tumorigenicity and ...

      Known for Prostate Cancer | Cells Bone | Cell Adhesion | C4 2 | Marrow Endothelial
      KOL-Index: 14839

      Novel recurrent gene fusions between the androgen-regulated gene TMPRSS2 and the ETS family members ERG, ETV1, or ETV4 have been recently identified as a common molecular event in prostate cancer development. We comprehensively analyzed the frequency and risk of disease progression for the TMPRSS2 and ETS family genes rearrangements in a cohort of 96 American men surgically treated for clinically localized prostate cancer. Using three break apart (TMPRSS2, ERG, ETV4) and one fusion ...

      Known for Tmprss2 Erg | Prostate Cancer | Etv1 Etv4 | Gene Aberrations | Clinically Localized
      KOL-Index: 14047

      Purpose We reported previously that the detection of androgen receptor splice variant-7 (AR-V7) mRNA in circulating tumor cells (CTCs) correlated with poor outcomes from the use of abiraterone and enzalutamide in patients with castration-resistant prostate cancer (CRPC). Here, we expanded our cohort size to better characterize the prognostic significance of AR-V7 in this setting. Methods We prospectively enrolled 202 patients with CRPC starting abiraterone or enzalutamide and ...

      Known for Clinical Significance | Messenger Receptors | Ctc Arv7 | Mrna Detection | Circulating Tumor Cells
      KOL-Index: 13144

      To delineate the role of SDF-1 and CXCR4 in metastatic prostate cancer (CaP), positive correlations were established between SDF-1 levels and tumor metastasis. Neutralization of CXCR4 limited the number and the growth of intraosseous metastasis in vivo. Together, these in vivo metastasis data provide critical support that SDF-1/CXCR4 plays a role in skeletal metastasis.

      INTRODUCTION: Previously we determined that the stromal-derived factor-1 (SDF-1)/CXCR4 chemokine axis is activated in ...

      Known for Sdf1 Cxcr4 | Prostate Cancer | Messenger Receptors | Metastasis Bone | Cap Cells
      KOL-Index: 13076

      Prostate-specific membrane antigen (PSMA)-targeted PET imaging has become commonly used in patients with prostate cancer (PCa). The PSMA reporting and data system version 1.0 (PSMA-RADS version 1.0) categorizes lesions on the basis of the likelihood of PCa involvement, with PSMA-RADS-3A (soft-tissue) and PSMA-RADS-3B (bone) lesions being indeterminate for the presence of disease. We retrospectively reviewed the imaging follow-up of such lesions to determine the rate at which they ...

      Known for Prostate Cancer | Lesions Psma | Pet Imaging | Version 10 | Retrospective Studies
      KOL-Index: 12610

      BACKGROUND: In virtually all patients with advanced prostate cancer, the disease metastasizes to bone and causes osteoblastic growth. However, the mechanisms that contribute to bone metastasis are poorly understood. It has been hypothesized that the bone provides a favorable growth environment for prostate cancer cells, which nonselectively seed the bone marrow from the bloodstream. Alternatively, prostate cancer cells may preferentially bind to bone marrow endothelial cells. We ...

      Known for Prostate Cancer Cells | Preferential Adhesion | Endothelial Cell | Bone Marrow | Vitro Assay
      KOL-Index: 12593

      PURPOSE: To evaluate the combination of intravenous (IV) paclitaxel, oral estramustine, and oral etoposide in patients with advanced hormone-refractory prostate cancer.

      PATIENTS AND METHODS: Forty patients with carcinoma of the prostate that was progressing despite hormonal therapy and who had undergone antiandrogen withdrawal (if previously treated with an antiandrogen) were enrolled onto this phase II trial. Patients were treated with oral estramustine 280 mg tid and oral etoposide 100 ...

      Known for Oral Etoposide | Patients Response | Prostate Cancer | Phase Trial | Life Qol
      KOL-Index: 12538

      CCL2 is a cytokine prevalent in the prostate cancer tumor microenvironment. Recently, we reported that CCL2 induces the mammalian target of rapamycin (mTOR) pathway to promote prostate cancer PC3 cell survival; however, the mechanism used by CCL2 to maintain mTOR complex-1 (mTORC1) activation requires clarification. This study demonstrates that upon serum starvation, CCL2 functions as a negative regulator of AMP-activated protein kinase (AMPK) by decreasing phosphorylation at its major ...

      Known for Cell Survival | Survivin Expression | Negative Regulator | Activated Protein | Cancer Pc3
      KOL-Index: 12226

      Epithelial-to-Mesenchymal Transition (EMT) and its reverse - Mesenchymal to Epithelial Transition (MET) - are hallmarks of cellular plasticity during embryonic development and cancer metastasis. During EMT, epithelial cells lose cell-cell adhesion and gain migratory and invasive traits either partially or completely, leading to a hybrid epithelial/mesenchymal (hybrid E/M) or a mesenchymal phenotype respectively. Mesenchymal cells move individually, but hybrid E/M cells migrate ...

      Known for Mesenchymal Phenotype | Hybrid Epithelial | Partial Emt | Tumor Cell | Cancer Metastasis

      Key People For Prostate Cancer

      Top KOLs in the world
      Ahmedin M Jemal
      united states breast cancer addis ababa
      Peter T Scardino
      prostate cancer active surveillance erectile function
      Rebecca L Siegel
      united states colorectal cancer incidence rates
      Johnathan I Jonathan
      prostate cancer gleason score needle biopsy
      Philip W Kantoff
      prostate cancer psma adc androgen deprivation therapy
      prostate cancer specific antigen pathological stage

      Kenneth J Pienta:Expert Impact

      Concepts for whichKenneth J Pientahas direct influence:Prostate cancer,  Cancer cells,  Nuclear matrix,  Tumor cells,  Cancer cell,  Bone marrow,  Prostate cancer cells,  Metastatic prostate cancer.

      Kenneth J Pienta:KOL impact

      Concepts related to the work of other authors for whichfor which Kenneth J Pienta has influence:Prostate cancer,  Tumor cells,  Gene expression,  Androgen receptor,  Cell proliferation,  Prostatic neoplasms,  Bone metastasis.



      Is this your profile? manage_accounts Claim your profile content_copy Copy URL code Embed Link to your profile

      The James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA, jhu.edu | Cellular and Molecular Medicine Program, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA;,

    Download on the App StoreGet it on Google Play

    Copyright © 2023 - KOL means Key Opinion Leaders .

    KOL does not provide medical advice, diagnosis or treatment.