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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
Molecular Cancer Research, ISSN 1541-7786, 04/2016, Volume 14, Issue 4, pp. 324 - 331
Journal Article
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 07/2013, Volume 123, Issue 7, pp. 2948 - 2960
Hormone therapies for advanced prostate cancer target the androgen receptor (AR) ligand-binding domain (LBD), but these ultimately fail and the disease... 
MEDICINE, RESEARCH & EXPERIMENTAL | SIGNAL-TRANSDUCTION PATHWAYS | CELLS | TRANSCRIPTIONAL ACTIVATION | PROTEIN | ANTIANDROGEN | GENE-EXPRESSION | TRANSACTIVATION DOMAIN | TUMOR-GROWTH | PROGRESSION | HORMONE RECEPTORS | Prostatic Neoplasms - metabolism | Stereoisomerism | Humans | Receptors, Androgen - metabolism | Transcriptional Activation - drug effects | Cercopithecus aethiops | Male | Androgen Receptor Antagonists - pharmacology | Benzhydryl Compounds - chemistry | Luciferases - genetics | Androgen Receptor Antagonists - chemistry | Receptors, Androgen - chemistry | Chlorohydrins - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Genes, Reporter | Prostatic Neoplasms - drug therapy | Protein Structure, Tertiary | Prostatic Neoplasms - pathology | Gene Expression | Antineoplastic Agents, Hormonal - pharmacology | Click Chemistry | Mice, SCID | Chlorohydrins - chemistry | Orchiectomy | Xenograft Model Antitumor Assays | Animals | Receptors, Androgen - genetics | Tumor Burden - drug effects | Protein Binding | Mice, Inbred NOD | Benzhydryl Compounds - pharmacology | Cell Proliferation - drug effects | Mice | Antineoplastic Agents, Hormonal - chemistry | COS Cells | Luciferases - biosynthesis | Antagonists (Biochemistry) | Care and treatment | Androgens | Physiological aspects | Prostate cancer | Health aspects | Methods | Cancer | Proteins | Medical research | Ligands | Kinases | Gene expression | Experiments | Drug dosages | Tumors
Journal Article
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
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
Journal of Clinical Oncology, ISSN 0732-183X, 08/2009, Volume 27, Issue 23, pp. 3742 - 3748
Journal Article