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Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. To... 
PATHWAY CHOICE | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | 53BP1 | CLASS-SWITCH RECOMBINATION | FANCONI-ANEMIA | DIFFERENTIAL EXPRESSION ANALYSIS | POLYMERASE-ZETA | TELOMERES | CELL BIOLOGY | Osteosarcoma - drug therapy | Mad2 Proteins - metabolism | Humans | Multiprotein Complexes | Ovarian Neoplasms - pathology | Bone Neoplasms - pathology | DNA Breaks, Double-Stranded | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | HEK293 Cells | Female | Bone Neoplasms - genetics | Ovarian Neoplasms - metabolism | Bone Neoplasms - drug therapy | BRCA1 Protein - deficiency | Telomere-Binding Proteins - metabolism | Ovarian Neoplasms - drug therapy | Osteosarcoma - metabolism | DNA-Binding Proteins | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinational DNA Repair | Tumor Suppressor p53-Binding Protein 1 - genetics | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Proteins - genetics | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Breast Neoplasms - genetics | Proteins - metabolism | Breast Neoplasms - pathology | Mad2 Proteins - genetics | Cell Line, Tumor | Mice | Osteosarcoma - genetics | Cell Cycle Proteins | Osteosarcoma - pathology | Care and treatment | DNA | Cancer cells | Breast cancer | Genetic aspects | Research | Gene expression | Single-stranded DNA | DNA damage | Homologous recombination | Poly(ADP-ribose) | Homology | Genomes | Inactivation | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Adenosine diphosphate | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Inhibitors | Prostate | Viability | Tumors | Telomere-Binding Proteins / metabolism | Osteosarcoma / genetics | Telomere-Binding Proteins / genetics | BRCA1 Protein / genetics | Cellular Biology | Genetics | Proteins / genetics | Osteosarcoma / drug therapy | Ovarian Neoplasms / genetics | Mad2 Proteins / genetics | Proteins / metabolism | Breast Neoplasms / drug therapy | Breast Neoplasms / metabolism | Tumor Suppressor p53-Binding Protein 1 / genetics | BRCA1 Protein / deficiency | Ovarian Neoplasms / metabolism | Mad2 Proteins / metabolism | Breast Neoplasms / pathology | Bone Neoplasms / genetics | Ovarian Neoplasms / pathology | Bone Neoplasms / pathology | Life Sciences | Bone Neoplasms / drug therapy | Ovarian Neoplasms / drug therapy | Osteosarcoma / metabolism | Biochemistry, Molecular Biology | Breast Neoplasms / genetics | Drug Resistance, Neoplasm / genetics | Osteosarcoma / pathology | Bone Neoplasms / metabolism | Poly(ADP-ribose) Polymerase Inhibitors / pharmacology | Cisplatin / pharmacology | Molecular biology | Tumor Suppressor p53-Binding Protein 1 / metabolism | Cancer
Journal Article
CA: a cancer journal for clinicians, ISSN 0007-9235, 2016, Volume 66, Issue 5, pp. 408 - 436
Answer questions and earn CME/CNE In this report, a team of surgical pathologists has provided a review of intraepithelial neoplasia in a host of (but not all)... 
carcinoma in situ | dysplasia | intraepithelial neoplasia | preinvasive neoplasia | precancer | HIGH-GRADE DYSPLASIA | URINARY-BLADDER | BARRETTS-ESOPHAGUS | HUMAN-PAPILLOMAVIRUS | INTRADUCTAL CARCINOMA | CARCINOMA IN-SITU | PAPILLARY UROTHELIAL HYPERPLASIA | ONCOLOGY | SINGLE ACADEMIC CENTER | TERM-FOLLOW-UP | NECK-CANCER IMPLICATIONS | Humans | Lung Neoplasms - metabolism | Ovarian Neoplasms - pathology | Lung Neoplasms - pathology | Male | Uterine Cervical Neoplasms - pathology | Head and Neck Neoplasms - metabolism | Breast Neoplasms - metabolism | Esophageal Neoplasms - pathology | Breast Neoplasms - therapy | American Cancer Society | Uterine Cervical Neoplasms - metabolism | Skin Neoplasms - diagnosis | Urinary Bladder Neoplasms - pathology | Female | Ovarian Neoplasms - metabolism | Uterine Cervical Neoplasms - therapy | Skin Neoplasms - pathology | Prostatic Neoplasms - pathology | Uterine Cervical Neoplasms - diagnosis | Skin Neoplasms - therapy | Carcinoma in Situ - pathology | Ovarian Neoplasms - diagnosis | Pancreatic Neoplasms - pathology | Risk Factors | Head and Neck Neoplasms - therapy | Lung Neoplasms - therapy | Carcinoma in Situ - therapy | Head and Neck Neoplasms - pathology | Skin Neoplasms - metabolism | Breast Neoplasms - pathology | Ovarian Neoplasms - therapy | Head and Neck Neoplasms - diagnosis | Breast Neoplasms - diagnosis | Carcinoma in Situ - diagnosis | Carcinoma in Situ - metabolism | Lung Neoplasms - diagnosis | Population Surveillance | Prevention | Care and treatment | Gastrointestinal system | Practice | Pathologists | Metastasis | Patients | Health aspects | Cervical cancer | Risk factors | Pathology | Usage | Diagnosis | Tumors | Medical diagnosis | Cancer
Journal Article
Nature medicine, ISSN 1546-170X, 2015, Volume 21, Issue 11, pp. 1262 - 1271
Cancer-associated muscle weakness is a poorly understood phenomenon, and there is no effective treatment. Here we find that seven different mouse models of... 
MEDICINE, RESEARCH & EXPERIMENTAL | CANCER CACHEXIA | CELLS | INTRACELLULAR CALCIUM | BIOCHEMISTRY & MOLECULAR BIOLOGY | RELEASE | CELL BIOLOGY | DYSTROPHIC MUSCLE | GROWTH-FACTOR-BETA | HORMONE-RELATED PROTEIN | RYANODINE RECEPTOR | CAMURATI-ENGELMANN-DISEASE | IN-VIVO | Neoplasms - metabolism | Prostatic Neoplasms - metabolism | Up-Regulation | Calcium - metabolism | Humans | Lung Neoplasms - metabolism | NADPH Oxidases - metabolism | Bone Neoplasms - secondary | Lung Neoplasms - pathology | Male | Muscle, Skeletal - metabolism | Osteolysis - etiology | Ryanodine Receptor Calcium Release Channel - metabolism | X-Ray Microtomography | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Neoplasms - complications | MCF-7 Cells | Osteolysis - diagnostic imaging | Muscle Proteins - metabolism | NADPH Oxidases - genetics | Female | Camurati-Engelmann Syndrome - metabolism | Muscle Strength | Calcium Signaling | Disease Models, Animal | Muscle Weakness - etiology | Prostatic Neoplasms - pathology | Oxidation-Reduction | Bone Neoplasms - diagnostic imaging | NADPH Oxidase 4 | Mice, SCID | Multiple Myeloma - metabolism | Absorptiometry, Photon | Osteolysis - metabolism | Multiple Myeloma - pathology | Animals | Muscle Contraction | Breast Neoplasms - pathology | Mice, Nude | Muscle Weakness - metabolism | Cell Line, Tumor | Mice | Neoplasms - pathology | Transforming Growth Factor beta - metabolism
Journal Article
Cancer research (Chicago, Ill.), ISSN 0008-5472, 04/2011, Volume 71, Issue 7, pp. 2600 - 2610
Journal Article
Metabolism, clinical and experimental, ISSN 0026-0495, 2015, Volume 64, Issue 2, pp. 182 - 189
Journal Article
Cancer cell, ISSN 1535-6108, 2012, Volume 21, Issue 5, pp. 642 - 654
Recent studies underscore the importance of myeloid cells in rendering distant organs hospitable for disseminating tumor cells to colonize. However, what... 
LUNG METASTASIS | STAT3 ACTIVATION | IMMUNE CELLS | ONCOLOGY | INFLAMMATION | IN-VIVO | NICHE | DEPENDENT TUMOR ANGIOGENESIS | CANCER | TUMORIGENESIS | PROGRESSION | CELL BIOLOGY | Neoplasms - metabolism | Prostatic Neoplasms - metabolism | Cell Proliferation | Lymph Nodes - pathology | Receptors, Lysosphingolipid - deficiency | Humans | Lung Neoplasms - metabolism | Tumor Microenvironment | Male | Prostatic Neoplasms - genetics | Lung Neoplasms - secondary | RNA Interference | Time Factors | STAT3 Transcription Factor - deficiency | Urinary Bladder Neoplasms - pathology | Receptors, Lysosphingolipid - genetics | Receptors, Lysosphingolipid - metabolism | Urinary Bladder Neoplasms - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Melanoma - metabolism | Skin Neoplasms - pathology | Prostatic Neoplasms - pathology | Transduction, Genetic | Signal Transduction | Cell Survival | Neoplasm Invasiveness | Lymph Nodes - metabolism | Lymphatic Metastasis | Melanoma - secondary | Mice, Knockout | Skin Neoplasms - metabolism | Animals | Cell Line, Tumor | CpG Islands | Myeloid Cells - metabolism | Mice | Myeloid Cells - pathology | Neoplasms - pathology | Cell Movement | Analysis | Oncology, Experimental | Transplantation | Metastasis | Research | Hematopoietic stem cells | Tumors | Cancer
Journal Article
Nature (London), ISSN 1476-4687, 2017, Volume 547, Issue 7664, pp. 453 - 457
... of polyunsaturated lipids. These lipids are the substrates for lipid peroxidation by lipoxygenase enzymes8,9. This lipid metabolism creates a dependency on pathways convergin... 
EPITHELIAL-MESENCHYMAL TRANSITION | METABOLISM | MULTIDISCIPLINARY SCIENCES | PROSTATE-CANCER | HUMAN-MELANOMA CELLS | SENSITIVITY | DEATH | INHIBITOR | EXPRESSION | SIGNATURE | REVEALS | Prostatic Neoplasms - metabolism | Cadherins - metabolism | Humans | Mesoderm - drug effects | Melanoma - enzymology | Male | Lipid Peroxides - metabolism | Zinc Finger E-box-Binding Homeobox 1 - genetics | Neoplasms - genetics | Mesoderm - enzymology | Cell Death | Epithelial-Mesenchymal Transition | Lipid Peroxidation - drug effects | Cell Transdifferentiation | Prostatic Neoplasms - drug therapy | Melanoma - metabolism | Glutathione Peroxidase - metabolism | Prostatic Neoplasms - pathology | Reproducibility of Results | Neoplasms - enzymology | Melanoma - pathology | Iron - metabolism | Neoplasms - drug therapy | Cell Lineage | Drug Resistance, Neoplasm - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Proteomics | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mesoderm - metabolism | Neoplasms - pathology | Mesoderm - pathology | Peroxidase | Research | Chemical properties | Chemical synthesis | Analysis | Cancer cells | Therapy | Biotechnology | Carcinoma | Mesenchyme | Genes | Lipid peroxidation | Lipids | Iron | Genomes | Phospholipids | Kinases | Cancer therapies | Proteins | Organoids | Dissipation | Peroxides | Lipid metabolism | Glutathione | Transfer RNA | Peroxidation | Glutathione peroxidase | Enzymes | Mortality | Melanoma | Selenocysteine | Tumor cell lines | Metabolism | Substrates | Cell death | Lipoxygenase | Prostate cancer | Prostate | Tumors | Apoptosis | Cancer | Index Medicus
Journal Article
European Urology, ISSN 0302-2838, 2016, Volume 71, Issue 3, pp. 313 - 316
Abstract STAT3 and its upstream activator IL6R have been implicated in the progression of prostate cancer and are possible future therapeutic targets. We... 
Urology | Tissue microarray | Castration-resistant | Prostate cancer | STAT3 | Metastases | CELLS | ACTIVATION | UROLOGY & NEPHROLOGY | RECEPTOR | BONE | Immunohistochemistry | Prostatic Neoplasms - metabolism | Humans | Transcriptome | Benzamides - metabolism | Bone Neoplasms - secondary | Male | Phosphoproteins - metabolism | Prostatic Neoplasms, Castration-Resistant - genetics | Prostatic Neoplasms, Castration-Resistant - pathology | Bone Neoplasms - metabolism | Neoplasm Metastasis | Adenocarcinoma - metabolism | Prostatic Neoplasms - genetics | Autopsy | Adenocarcinoma - genetics | Bone Neoplasms - genetics | Liver Neoplasms - secondary | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Prostatic Neoplasms - pathology | Liver Neoplasms - genetics | Piperidines - metabolism | Receptors, Interleukin-6 - genetics | Lymph Nodes - metabolism | Lymphatic Metastasis | Prostatic Neoplasms, Castration-Resistant - metabolism | Adenocarcinoma - secondary | Liver Neoplasms - metabolism | Receptors, Interleukin-6 - metabolism | RNA | Analysis | Genes | Genetic research | Development and progression | Metastasis | Gene expression | Proteins | Medical research | Medicine, Experimental | Urologi och njurmedicin | Medical and Health Sciences | Medicin och hälsovetenskap | Klinisk medicin | Clinical Medicine | Cancer and Oncology | Urology and Nephrology | Cancer och onkologi
Journal Article
European urology, ISSN 0302-2838, 2015, Volume 67, Issue 1, pp. 53 - 60
Abstract Background Enzalutamide is a novel antiandrogen with proven efficacy in metastatic castration-resistant prostate cancer (mCRPC). Objective To evaluate... 
Urology | Castration-resistant prostate cancer | Primary resistance to enzalutamide | Androgen signaling inhibition | Bone metastasis | Bone tumor microenvironment | Adaptive feedback mechanism | Androgen receptor | Predictors of outcome | Enzalutamide | Tissue-based research | TESTOSTERONE | CHEMOTHERAPY | RECEPTOR SPLICE VARIANTS | THERAPY | DEPRIVATION | CLINICAL-TRIALS | UROLOGY & NEPHROLOGY | INCREASED SURVIVAL | PROGRESSION | ABIRATERONE | Prospective Studies | Phenylthiohydantoin - therapeutic use | Humans | Middle Aged | Receptors, Androgen - metabolism | Retroviridae Proteins, Oncogenic - metabolism | Bone Neoplasms - secondary | Cytoplasm - metabolism | Drug Resistance, Neoplasm | Ki-67 Antigen - metabolism | Male | Antineoplastic Agents - therapeutic use | Receptors, Glucocorticoid - metabolism | Prostatic Neoplasms, Castration-Resistant - pathology | Bone Neoplasms - metabolism | Cell Nucleus - metabolism | Protein Isoforms - metabolism | Bone Marrow - metabolism | Aged, 80 and over | Adult | Bone Neoplasms - drug therapy | Testosterone - blood | Gene Dosage | Prostatic Neoplasms, Castration-Resistant - drug therapy | Prostatic Neoplasms, Castration-Resistant - metabolism | Bone Marrow Neoplasms - secondary | Phenylthiohydantoin - analogs & derivatives | Prostate-Specific Antigen - blood | Receptors, Androgen - genetics | Signal Transduction - drug effects | Bone Marrow Neoplasms - metabolism | Aged | Bone Marrow Neoplasms - drug therapy | Steroid 17-alpha-Hydroxylase - metabolism | Prostate cancer | Metastasis | Bone marrow biopsy | Androgen | Antiandrogens
Journal Article