A5028617589- Prostate Cancer Treatment and Research
- Microtubule and mitosis dynamics
- Circadian rhythm and melatonin
- Genetics, Aging, and Longevity in Model Organisms
- Cancer, Stress, Anesthesia, and Immune Response
- Prostate Cancer Diagnosis and Treatment
- Urinary Bladder and Prostate Research
- TGF-β signaling in diseases
- Hormonal and reproductive studies
- Cell death mechanisms and regulation
- Cancer, Lipids, and Metabolism
- Cell Adhesion Molecules Research
- Estrogen and related hormone effects
- Cancer-related Molecular Pathways
- Quinazolinone synthesis and applications
- Hippo pathway signaling and YAP/TAZ
- Extracellular vesicles in disease
- Epigenetics and DNA Methylation
- Cancer therapeutics and mechanisms
- MicroRNA in disease regulation
- Photoreceptor and optogenetics research
- Historical and Scientific Studies
- Synthesis of Tetrazole Derivatives
- Inflammatory mediators and NSAID effects
- COVID-19 and healthcare impacts
Icahn School of Medicine at Mount Sinai
2020-2025
University of Kentucky
2003-2023
Tisch Hospital
2021-2023
Tisch Cancer Institute
2021-2023
Johns Hopkins University
1987-2021
John Wiley & Sons (United States)
2016-2021
Johns Hopkins Medicine
1987-2021
Sidney Kimmel Comprehensive Cancer Center
2019-2021
New York Proton Center
2020
Mount Sinai Medical Center
2020
Castration-induced androgen deprivation leads to the activation of programmed death androgen-dependent prostatic epithelial cells in rat ventral prostate. In order identify potential mediators this cell death, expression transforming growth factor-β (TGFβ) prostate was studied, after castration induced-androgen withdrawal. Steady state levels TGFβ mRNA were determined by Northern blot analysis and compared with for prostatein C3, major secretory protein also TRPM-2, a gene that is...
The ability of transforming growth factor B1 (TGFβ1) to inhibit proliferation and activate death rat ventral prostatic glandular cells was tested both in vivo vitro. In administration 50 ng TGFβ1/day directly the regressed prostate previously castrated male rats had no effect on proliferative regrowth induced by exogeneous androgen replacement. addition, androgen- stimulated cell vitro organ culture not affected exposure 0.1–20 ng/ml TGFβ1. contrast intact noncastrated resulted about 25%...
Scatchard analyses of the binding transforming growth factor-beta (TGF beta) to membranes from rat ventral prostate revealed presence high affinity (Kd = 140 pM) saturable sites for [125I]TGF beta. The beta prostatic membranes, while displaced in excess unlabeled TGF beta, is unaffected by epidermal factor, nerve fibroblast or insulin, indicating specificity binding. Affinity labeling these membrane receptors covalent attachment with bis-(sulfosuccinimidyl)suberate and subsequent...
Prostate cancer is a highly heterogeneous disease. Progression on androgen deprivation therapy (ADT) to castration-resistant (CRPC), or neuroendocrine prostate (NEPC), associated with poor patient survival. This comment highlights recent evidence the epigenetic mechanisms underlying emergence of lineage plasticity and differentiation in treatment-resistant tumors.
ABSTRACT: Androgen‐dependent normal prostatic glandular cells and androgen‐dependent cancer can be induced to undergo cell death after androgen ablation. This does not require the proliferate occurs as an energy‐dependent process collectively referred “programmed death” in which actively commit “suicide.” Associated with this programmed pathway is enhanced expression of a series genes fragmentation genomic DNA into nucleosomal oligomers. irreversible commitment step results from activation...
In this study we evaluated the effect of over-expression bcl-2 gene, a potent apoptosis suppressor, on radiation-induced apoptotic cell death in 2 human prostate cancer lines, androgen-independent PC-3 cells and androgen-sensitive LNCaP cells. Cells were transfected with gene transfectant clones isolated under neomycin selection; integration level mRNA protein expression cloned transfectants examined by Southern, Northern Western blot analyses, respectively. Parental, neo control...
When defined in terms of markers for normal cell lineages, most invasive breast cancer cells correspond to the phenotype common luminal epithelial found terminal ductal lobular units. Luminal cultured from milk, which have limited proliferative potential, now been immortalized by introducing gene encoding simian virus 40 large tumor (T) antigen. Infection with a recombinant retrovirus proved be 50-100 times more efficient than calcium phosphate transfection, and 17 lines isolated, only 5...
No AccessJournal of UrologyClinical Urology: Original Articles1 Jun 1998INDUCTION OF PROSTATE APOPTOSIS BY DOXAZOSIN IN BENIGN PROSTATIC HYPERPLASIA NATASHA KYPRIANOU, JUAN P. LITVAK, ANDREW BORKOWSKI, RICHARD ALEXANDER, and STEPHEN C. JACOBS KYPRIANOUNATASHA KYPRIANOU , LITVAKJUAN LITVAK BORKOWSKIANDREW BORKOWSKI ALEXANDERRICHARD ALEXANDER JACOBSSTEPHEN View All Author Informationhttps://doi.org/10.1016/S0022-5347(01)63162-8AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack...
No AccessJournal of UrologyInvestigative Urology1 Jun 1999alpha1-ADRENOCEPTOR ANTAGONISTS TERAZOSIN AND DOXAZOSIN INDUCE PROSTATE APOPTOSIS WITHOUT AFFECTING CELL PROLIFERATION IN PATIENTS WITH BENIGN PROSTATIC HYPERPLASIA JOANNA K. CHON, ANDREW BORKOWSKI, ALAN W. PARTIN, JOHN T. ISAACS, STEPHEN C. JACOBS, and NATASHA KYPRIANOU CHONJOANNA CHON , BORKOWSKIANDREW BORKOWSKI PARTINALAN PARTIN ISAACSJOHN ISAACS JACOBSSTEPHEN JACOBS KYPRIANOUNATASHA View All Author...
Transforming growth factor-beta (TGF-beta1) is a potent negative regulator of cell that transduces signals through interactions with type I and II receptors. Abnormal expression mutational alterations these receptors have been observed in several human malignancies. In this study, we investigated the two types TGF-beta1 receptors, R-I R-II, normal prostate, primary prostate adenocarcinoma lymph nodes metastatic deposits. Expression receptor proteins was examined by immunohistochemical...
Abstract Despite progress in prostate cancer (PC) therapeutics, distant metastasis remains a major cause of morbidity and mortality from PC. Thus, there is growing recognition that preventing or delaying PC holds great potential for substantially improving patient outcomes. Here we show receptor-interacting protein kinase 2 (RIPK2) clinically actionable target inhibiting metastasis. RIPK2 amplified/gained ~65% lethal metastatic castration-resistant Its overexpression associated with disease...