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Nature, ISSN 0028-0836, 07/2015, Volume 523, Issue 7560, pp. 347 - 351
Prostate cancer resistance to castration occurs because tumours acquire the metabolic capability of converting precursor steroids to 5... 
ANDROGEN RECEPTOR | 3-BETA-HYDROXYSTEROID DEHYDROGENASE | CYP17A1 INHIBITION | MECHANISM | TESTOSTERONE | RATIONALE | MULTIDISCIPLINARY SCIENCES | INCREASED SURVIVAL | CHEMOTHERAPY | EXPOSURE | ENZALUTAMIDE | Chromatin - metabolism | Prostatic Neoplasms - metabolism | Steroid 17-alpha-Hydroxylase - antagonists & inhibitors | Androgen Receptor Antagonists - therapeutic use | Humans | Receptors, Androgen - metabolism | Gene Expression Regulation, Neoplastic | Androgens - biosynthesis | Male | Androstenes - pharmacology | Androgen Receptor Antagonists - pharmacology | 3-Hydroxysteroid Dehydrogenases - antagonists & inhibitors | Biotransformation | Cell Division | 3-Oxo-5-alpha-Steroid 4-Dehydrogenase - metabolism | 3-Hydroxysteroid Dehydrogenases - metabolism | Prostatic Neoplasms - drug therapy | Dihydrotestosterone - metabolism | Phenylthiohydantoin - pharmacology | Prostatic Neoplasms - pathology | Androstenes - therapeutic use | 5-alpha Reductase Inhibitors - therapeutic use | Prostatic Neoplasms, Castration-Resistant - drug therapy | Phenylthiohydantoin - analogs & derivatives | Androgen Receptor Antagonists - metabolism | Xenograft Model Antitumor Assays | Androstenes - chemistry | Animals | Biosynthetic Pathways - drug effects | Survival Analysis | 5-alpha Reductase Inhibitors - pharmacology | Androstenes - metabolism | Prostatic Neoplasms - enzymology | Mice | Steroid 17-alpha-Hydroxylase - metabolism | 5-alpha Reductase Inhibitors - metabolism | Androgens - metabolism | Enzymes | Testosterone | Androgens | Metabolites | Ligands | Gene expression | Prostate cancer | Tumors
Journal Article
Science, ISSN 0036-8075, 5/2009, Volume 324, Issue 5928, pp. 787 - 790
Metastatic prostate cancer is treated with drugs that antagonize androgen action, but most patients progress to a more aggressive form of the disease called... 
COS cells | Androgens | Cell lines | Agonists | Oncology | Reports | Androgen antagonists | Prostate cancer | Heterologous transplantation | Tumors | Vehicles | NONSTEROIDAL ANTIANDROGENS | STRUCTURAL BASIS | AFFINITY | MULTIDISCIPLINARY SCIENCES | ANDROGEN-RECEPTOR | RESISTANCE | ANTAGONISM | LIGAND | MODEL | BICALUTAMIDE | Transcription, Genetic - drug effects | Nitriles - pharmacology | Phenylthiohydantoin - therapeutic use | Humans | Receptors, Androgen - metabolism | Biological Availability | Male | Antineoplastic Agents - therapeutic use | Tosyl Compounds - pharmacology | Antineoplastic Agents - metabolism | Cell Nucleus - metabolism | Receptors, Androgen - chemistry | Antineoplastic Agents - pharmacokinetics | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Prostatic Neoplasms - drug therapy | Androgen Antagonists - pharmacokinetics | Phenylthiohydantoin - pharmacology | Nitriles - metabolism | Prostatic Neoplasms - pathology | Androgen Antagonists - metabolism | Androgen Antagonists - pharmacology | Anilides - metabolism | DNA - metabolism | Phenylthiohydantoin - analogs & derivatives | Xenograft Model Antitumor Assays | Animals | Receptors, Androgen - genetics | Anilides - pharmacology | Tosyl Compounds - metabolism | Androgen Antagonists - therapeutic use | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Phenylthiohydantoin - metabolism | Drug Screening Assays, Antitumor | Phenylthiohydantoin - pharmacokinetics | Care and treatment | Antiandrogens | Dosage and administration | Drug therapy | Methods | Cancer | Chemotherapy | Pharmacology | Binding sites
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 5, pp. 575 - 586
Prostate cancer is characterized by its dependence on androgen receptor (AR) and frequent activation of PI3K signaling. We find that AR transcriptional output... 
TARGET | CELLS | ONCOLOGY | PATHWAY | DUAL PI3K/MTOR INHIBITOR | KINASE | TUMOR-SUPPRESSOR | AKT | INDUCTION | MTOR COMPLEX | HORMONAL-THERAPY | CELL BIOLOGY | Receptor, ErbB-3 - metabolism | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Phosphoprotein Phosphatases - metabolism | Receptors, Androgen - metabolism | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Male | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Prostatic Neoplasms - genetics | Receptors, Androgen - drug effects | Transfection | RNA Interference | Time Factors | Transcription, Genetic | Receptor, ErbB-2 - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Genes, Reporter | Prostatic Neoplasms - drug therapy | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | PTEN Phosphohydrolase - deficiency | Androgen Antagonists - pharmacology | Receptor, ErbB-3 - antagonists & inhibitors | Mice, Transgenic | Nuclear Proteins - metabolism | Mice, SCID | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Xenograft Model Antitumor Assays | Magnetic Resonance Imaging | Feedback, Physiological | Animals | Signal Transduction - drug effects | Tumor Burden - drug effects | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Phosphatases | Health aspects | Phosphotransferases | Prostate cancer | Analysis | Tumors
Journal Article
Cancer Research, ISSN 0008-5472, 12/2014, Volume 74, Issue 23, pp. 7103 - 7114
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2011, Volume 108, Issue 9, pp. 3755 - 3760
Growth hormone-releasing hormone (GHRH), a hypothalamic polypeptide, acts as a potent autocrine/paracrine growth factor in many cancers. Benign prostatic... 
Hormone antagonists | Receptors | Cell growth | Cytokines | Epithelial cells | Genes | Prostatic hyperplasia | Hormones | Prostate | Apoptosis | Rodent benign prostatic hyperplasia model | Prostatic hypertrophy | Chronic prostatic inflammation | Prostatic cell death | CYCLOOXYGENASE-2 | MULTIDISCIPLINARY SCIENCES | prostatic cell death | PROLIFERATION | rodent benign prostatic hyperplasia model | COMBINATION | SPLICE VARIANTS | CANCER | INHIBITION | THERAPY | prostatic hypertrophy | CELL LUNG-CARCINOMA | INFLAMMATION | chronic prostatic inflammation | EXPRESSION | Immunohistochemistry | Transcription, Genetic - drug effects | Prostatic Hyperplasia - pathology | Sermorelin - administration & dosage | Apoptosis - drug effects | Humans | Receptors, Androgen - metabolism | Male | NF-kappa B - metabolism | Receptors, Neuropeptide - metabolism | Prostate - metabolism | Inflammation - complications | Prostate - pathology | Interleukin-1beta - metabolism | Receptors, Pituitary Hormone-Regulating Hormone - metabolism | Inflammation Mediators - metabolism | Sermorelin - pharmacology | Prostate - drug effects | Sermorelin - analogs & derivatives | Gene Expression Regulation, Neoplastic - drug effects | Receptors, Pituitary Hormone-Regulating Hormone - genetics | Rats | Receptors, Neuropeptide - genetics | Signal Transduction - genetics | Down-Regulation - drug effects | Growth Hormone-Releasing Hormone - genetics | Prostatic Hyperplasia - genetics | Cell Division - drug effects | Prostate-Specific Antigen - blood | Growth Hormone-Releasing Hormone - metabolism | Organ Size - drug effects | Alternative Splicing - drug effects | Animals | Signal Transduction - drug effects | Cyclooxygenase 2 - metabolism | Inflammation - genetics | Prostatic Hyperplasia - blood | Prostatic Hyperplasia - enzymology | Growth Hormone-Releasing Hormone - antagonists & inhibitors | Insulin-Like Growth Factor I - metabolism | Genetic aspects | Polypeptides | Somatotropin releasing hormone | Health aspects | Hypertrophy | Biological Sciences
Journal Article
Journal Article
Environmental Health Perspectives, ISSN 0091-6765, 8/2011, Volume 119, Issue 8, pp. 1142 - 1148
Background: The large and increasing number of chemicals released into the environment demands more efficient and cost-effective approaches for assessing... 
Chemical hazards | Receptors | Genomics | Environmental health | Agonists | Ligands | Cytotoxicity | Libraries | Environmental agencies | Research | Nuclear receptors | Chemical genomics | qHTS | Assay performance | Tox21 | assay performance | TOXICITY | ANTAGONISM | IDENTIFICATION | ESTROGEN-RECEPTOR | nuclear receptors | ENVIRONMENTAL SCIENCES | IN-VITRO | PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH | EVOLUTION | DISEASE | ASSAYS | SUPERFAMILY | HEALTH | chemical genomics | cytotoxicity | Peroxisome Proliferator-Activated Receptors - agonists | Cell Line | Retinoid X Receptor alpha - metabolism | Peroxisome Proliferator-Activated Receptors - antagonists & inhibitors | Humans | Orphan Nuclear Receptors - agonists | Receptors, Androgen - metabolism | Receptors, Cytoplasmic and Nuclear - agonists | Orphan Nuclear Receptors - metabolism | PPAR gamma - metabolism | Receptors, Thrombin - antagonists & inhibitors | Retinoid X Receptor alpha - agonists | Fragile X Mental Retardation Protein | Orphan Nuclear Receptors - antagonists & inhibitors | Retinoid X Receptor alpha - antagonists & inhibitors | PPAR gamma - antagonists & inhibitors | Receptors, Thrombin - agonists | Liver X Receptors | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Peroxisome Proliferator-Activated Receptors - metabolism | Receptors, Thrombin - metabolism | Estrogen Receptor alpha - metabolism | Environmental Pollutants - toxicity | Receptors, Cytoplasmic and Nuclear - metabolism | Environmental aspects | Physiological aspects | Cell receptors | Health aspects | Chemicals | Index Medicus
Journal Article
Molecular Endocrinology, ISSN 0888-8809, 05/2012, Volume 26, Issue 5, pp. 716 - 735
Recently, we have identified serum response factor (SRF) as a mediator of clinically relevant androgen receptor (AR) action in prostate cancer (PCa). Genes... 
THERAPY | REMAINS HORMONE DRIVEN | ENDOCRINOLOGY & METABOLISM | NUCLEOTIDE EXCHANGE FACTOR | SERUM RESPONSE FACTOR | RECEPTOR | KINASE INHIBITOR | CASTRATION | COREGULATOR EXPRESSION | PROGRESSION | SMALL-MOLECULE INHIBITOR | Humans | Male | Neoplasm Proteins - antagonists & inhibitors | rhoA GTP-Binding Protein - metabolism | Protein Transport - drug effects | Promoter Regions, Genetic - drug effects | Prostate - pathology | Cell Nucleus - metabolism | rho-Associated Kinases - metabolism | Prostate - drug effects | Neoplasm Proteins - genetics | Recombinant Proteins - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | rhoA GTP-Binding Protein - antagonists & inhibitors | Muscle Proteins - genetics | Receptors, Androgen - genetics | Androgens - pharmacology | Signal Transduction - drug effects | Mice, Nude | Mice | Prostatic Neoplasms - metabolism | Oncogene Proteins, Fusion - metabolism | LIM-Homeodomain Proteins - metabolism | Receptors, Androgen - metabolism | rhoA GTP-Binding Protein - genetics | Neoplasm Proteins - metabolism | Prostate - metabolism | rho-Associated Kinases - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Muscle Proteins - metabolism | Androgens - adverse effects | Gene Expression Regulation, Neoplastic - drug effects | Recombinant Proteins - metabolism | Prostatic Neoplasms - pathology | Prostatic Neoplasms - surgery | Trans-Activators | Neoplasm Recurrence, Local | rho-Associated Kinases - genetics | Recombinant Proteins - agonists | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | LIM-Homeodomain Proteins - genetics | Animals | Neoplasm Proteins - agonists | Oncogene Proteins, Fusion - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | rhoA GTP-Binding Protein - agonists | Cell Nucleus - drug effects | Original Research
Journal Article
Nature Medicine, ISSN 1078-8956, 09/2017, Volume 23, Issue 9, pp. 1055 - 1062
Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising anticancer therapies. The gene encoding the E3 ubiquitin ligase... 
SELECTIVE-INHIBITION | TARGET | MEDICINE, RESEARCH & EXPERIMENTAL | ANDROGEN RECEPTOR | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACUTE MYELOID-LEUKEMIA | ENHANCERS | CELL BIOLOGY | RNA-SEQ | BROMODOMAIN INHIBITION | MUTATIONS | BRD4 | Prostatic Neoplasms - metabolism | Immunoprecipitation | TOR Serine-Threonine Kinases - metabolism | Humans | Drug Resistance, Neoplasm | Male | Gene Expression Profiling | Molecular Targeted Therapy | Mechanistic Target of Rapamycin Complex 1 | Transcription Factors - drug effects | Multiprotein Complexes - metabolism | Prostatic Neoplasms - genetics | Proteasome Endopeptidase Complex - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Nuclear Proteins - drug effects | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Multiprotein Complexes - drug effects | Prostatic Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | RNA-Binding Proteins - antagonists & inhibitors | Triazoles - therapeutic use | Cell Survival | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Azepines - therapeutic use | RNA-Binding Proteins - drug effects | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Nuclear Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | RNA-Binding Proteins - metabolism | rac1 GTP-Binding Protein - metabolism | Proto-Oncogene Proteins c-akt - drug effects | rac1 GTP-Binding Protein - genetics | Gene mutations | Physiological aspects | Genetic aspects | Research | Drug resistance | Drug therapy | Prostate cancer | Ubiquitin | Inhibitor drugs | Stabilization | AKT protein | Activation | Biosynthesis | Degradation | Proteins | Ubiquitination | Transcription activation | Ubiquitin-protein ligase | Binding | Rac1 protein | Tumor cell lines | Gene expression | Cholesterol | Mutants | Inhibitors | Proteasomes | Biomarkers | Bet protein | Prostate | Cancer | Guanosinetriphosphatase
Journal Article
Endocrinology, ISSN 0013-7227, 09/2013, Volume 154, Issue 9, pp. 3294 - 3304
Gonadal steroids are potent regulators of adult neurogenesis. We previously reported that androgens, such as testosterone (T) and dihydrotestosterone (DHT),... 
SPINAL NUCLEUS | FEMALE RATS | TESTOSTERONE | ENDOCRINOLOGY & METABOLISM | PROMOTES SURVIVAL | CELL-PROLIFERATION | GRANULE CELLS | HIPPOCAMPAL NEUROGENESIS | NEWBORN NEURONS | BRAIN | INSENSITIVITY | Castration - adverse effects | Neuroprotective Agents - therapeutic use | Neurons - pathology | Microtubule-Associated Proteins - metabolism | Neuroprotective Agents - antagonists & inhibitors | Receptors, Androgen - metabolism | Testosterone Propionate - antagonists & inhibitors | Male | Neurons - cytology | Neural Stem Cells - cytology | Hormone Replacement Therapy | Neuroprotective Agents - metabolism | Neuroprotective Agents - pharmacology | Dentate Gyrus - drug effects | Androgens - therapeutic use | Receptors, Androgen - chemistry | Neurogenesis - drug effects | Neurons - metabolism | Neurons - drug effects | Androgen Antagonists - toxicity | Mutant Proteins - antagonists & inhibitors | Drug Resistance | Biomarkers - metabolism | Cell Survival - drug effects | Testosterone Propionate - pharmacology | Dentate Gyrus - metabolism | Androgen-Insensitivity Syndrome - drug therapy | Neural Stem Cells - drug effects | Rats | Mutant Proteins - metabolism | Neuropeptides - metabolism | Neural Stem Cells - pathology | Rats, Sprague-Dawley | Dentate Gyrus - cytology | Animals | Receptors, Androgen - genetics | Androgens - pharmacology | Signal Transduction - drug effects | Androgen-Insensitivity Syndrome - metabolism | Androgen-Insensitivity Syndrome - chemically induced | Androgens - chemistry | Androgens - metabolism | Dentate Gyrus - pathology | Neural Stem Cells - metabolism | Testosterone Propionate - therapeutic use | Mutant Proteins - agonists
Journal Article