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Nature, ISSN 0028-0836, 01/2016, Volume 529, Issue 7586, pp. 413 - 417
Triple-negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy(1-3). BET bromodomain... 
SELECTIVE-INHIBITION | SUPER-ENHANCERS | RNA-SEQ | SUBTYPES | INFLAMMATION | STRATEGY | MULTIDISCIPLINARY SCIENCES | CELL IDENTITY | C-MYC | PP2A | LEUKEMIA | Chromatin - metabolism | Transcription, Genetic - drug effects | Humans | Transcription Factors - deficiency | Triple Negative Breast Neoplasms - drug therapy | Genome, Human - drug effects | Nuclear Proteins - deficiency | Protein Binding - drug effects | Triple Negative Breast Neoplasms - pathology | Female | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Nuclear Proteins - genetics | Triazoles - therapeutic use | Cell Proliferation - genetics | Mediator Complex Subunit 1 - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Phosphoserine - metabolism | Genome, Human - genetics | Azepines - therapeutic use | Azepines - pharmacology | Binding, Competitive - drug effects | Transcription Factors - metabolism | Triazoles - pharmacology | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Triple Negative Breast Neoplasms - genetics | Epigenesis, Genetic - genetics | Triple Negative Breast Neoplasms - metabolism | Nuclear Proteins - antagonists & inhibitors | Protein Phosphatase 2 - metabolism | Proteomics | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Chromatin - genetics | Casein Kinase II - metabolism | Drug Resistance, Neoplasm - drug effects | Protein Structure, Tertiary - drug effects | Antimitotic agents | Enzyme inhibitors | Patient outcomes | Breast cancer | Dosage and administration | Drug therapy | Antineoplastic agents | Studies | Inhibitor drugs | Drug resistance | Gene expression | Drug dosages | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 06/2017, Volume 546, Issue 7658, pp. 431 - 435
Therapies that target signalling molecules that are mutated in cancers can often have substantial short-term effects, but the emergence of resistant cancer... 
METASTATIC MELANOMA | BRAF INHIBITOR | SUBPOPULATIONS | CHROMATIN | MULTIDISCIPLINARY SCIENCES | SINGLE MAMMALIAN-CELLS | STATE | MECHANISMS | MUTATIONS | VEMURAFENIB | PLASTICITY | Transcription, Genetic - drug effects | Humans | Male | Transcription Factor AP-1 - metabolism | DNA-Binding Proteins - metabolism | Melanoma - genetics | Female | Indoles - pharmacology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Single-Cell Analysis | Cellular Reprogramming - genetics | ErbB Receptors - metabolism | In Situ Hybridization, Fluorescence | Nuclear Proteins - metabolism | Signal Transduction - genetics | Melanoma - pathology | Sulfonamides - pharmacology | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Genetic Markers - drug effects | Vemurafenib | Drug Resistance, Neoplasm - genetics | Animals | Signal Transduction - drug effects | Genetic Markers - genetics | Cell Line, Tumor | Oncogene Protein p65(gag-jun) - metabolism | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Antimitotic agents | Cell interaction | Dosage and administration | Antineoplastic agents | Drug resistance | Observations | Health aspects | Subpopulations | Transcription factors | Substance abuse treatment | Variability | Activator protein 1 | Melanoma | Genomes | Kinases | Gene expression | Sox10 protein | Signal transduction | Signaling | Converting | Population | Mutation | Differentiation | Deoxyribonucleic acid--DNA | Cancer | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 514, Issue 7521, pp. 247 - 251
The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types(1). However, loss-of-function mutations in PRC2 components occur in a... 
SUPPRESSOR | GENE | MULTIDISCIPLINARY SCIENCES | MICE | NF1 MICRODELETION PATIENTS | MUTATIONS | BET BROMODOMAIN INHIBITION | CANCER | TUMORS | NEUROFIBROMATOSIS TYPE-1 | EZH2 | Chromatin - metabolism | Transcription, Genetic - drug effects | Polycomb Repressive Complex 2 - genetics | Humans | Transcription Factors - deficiency | ras Proteins - metabolism | Neurofibromin 1 - deficiency | Glioma - genetics | Neoplasms - genetics | Melanoma - genetics | Tumor Suppressor Proteins - deficiency | Glioma - pathology | Nerve Sheath Neoplasms - pathology | Nuclear Proteins - deficiency | Tumor Suppressor Proteins - genetics | Epigenesis, Genetic - drug effects | Cell Death - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Nuclear Proteins - genetics | Chromatin - drug effects | Nerve Sheath Neoplasms - drug therapy | Disease Models, Animal | Triazoles - therapeutic use | Nerve Sheath Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | ras Proteins - antagonists & inhibitors | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Melanoma - pathology | Transcription Factors - genetics | Azepines - therapeutic use | Neoplasms - drug therapy | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Animals | Polycomb Repressive Complex 2 - deficiency | Melanoma - drug therapy | Nuclear Proteins - antagonists & inhibitors | Mice | Neoplasms - pathology | Polycomb Repressive Complex 2 - metabolism | Chromatin - genetics | Neurofibromin 1 - genetics | Glioma - drug therapy | Epigenetic inheritance | Ras genes | Genetic transcription | Research | Gliomas | Studies | Mutation | Genes | Tumors | Defects | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7570, pp. 538 - 542
Bromodomain and extra terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a newtherapeutic opportunity by directly targeting... 
SELECTIVE-INHIBITION | ACCURATE | CHROMATIN | MECHANISM | MULTIDISCIPLINARY SCIENCES | ACUTE MYELOID-LEUKEMIA | DRUG-RESISTANCE | MUTATIONS | SEQUENCING DATA | CANCER | DISCOVERY | Chromatin - metabolism | Transcription, Genetic - drug effects | Clone Cells - drug effects | Neoplastic Stem Cells - drug effects | Epigenesis, Genetic | Humans | Leukemia, Myeloid, Acute - metabolism | Molecular Targeted Therapy | Neoplastic Stem Cells - metabolism | Leukemia, Myeloid, Acute - drug therapy | Neoplastic Stem Cells - pathology | Gene Expression Regulation, Neoplastic - drug effects | Hematopoietic Stem Cells - drug effects | Benzodiazepines - pharmacology | Leukemia, Myeloid, Acute - pathology | Cells, Cultured | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Hematopoietic Stem Cells - metabolism | Clone Cells - metabolism | beta Catenin - metabolism | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Clone Cells - pathology | Wnt Signaling Pathway - drug effects | Genes, myc - genetics | Hematopoietic Stem Cells - cytology | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Drug Resistance, Neoplasm - drug effects | Leukemia, Myeloid, Acute - genetics | Proteins | Leukemia | Cloning | Cell cycle | Stem cells | Epigenetics | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7570, pp. 543 - 547
Journal Article
PLoS Genetics, ISSN 1553-7390, 09/2010, Volume 6, Issue 9, pp. e1001102 - e1001102
Journal Article
Science, ISSN 0036-8075, 8/2013, Volume 341, Issue 6146, pp. 651 - 654
Journal Article
Developmental Cell, ISSN 1534-5807, 2002, Volume 3, Issue 6, pp. 889 - 901
Signaling by RANKL is essential for terminal differentiation of monocytes/mcrophages into osteoclasts. The TRAF6 and c-Fos signaling pathways both play... 
LYMPH-NODE ORGANOGENESIS | CELLS | CYCLOSPORINE-A | OSTEOPROTEGERIN-LIGAND | KEY REGULATOR | C-FOS | RECEPTOR ACTIVATOR | GENE-EXPRESSION | DEVELOPMENTAL BIOLOGY | OSTEOPETROSIS | NF-KAPPA-B | CELL BIOLOGY | Transcription, Genetic - drug effects | Genetic Testing | Membrane Glycoproteins - metabolism | Oligonucleotide Array Sequence Analysis | RANK Ligand | Osteoclasts - cytology | Promoter Regions, Genetic - drug effects | RNA, Messenger - metabolism | Calcineurin - genetics | Cell Culture Techniques | Active Transport, Cell Nucleus - genetics | Signal Transduction - genetics | Nuclear Proteins | Signal Transduction - drug effects | Calcium Signaling - drug effects | Active Transport, Cell Nucleus - drug effects | Hematopoietic Stem Cells - cytology | Proto-Oncogene Proteins c-fos - genetics | Mice | Transcription, Genetic - genetics | Calcium Signaling - genetics | Receptor Activator of Nuclear Factor-kappa B | Transcription Factors - deficiency | Promoter Regions, Genetic - genetics | DNA-Binding Proteins - deficiency | Cell Differentiation - genetics | Carrier Proteins - pharmacology | Hematopoietic Stem Cells - drug effects | Gene Expression Regulation - genetics | Membrane Glycoproteins - pharmacology | Mice, Inbred C57BL | Cells, Cultured | Proto-Oncogene Proteins c-fos - metabolism | Hematopoietic Stem Cells - metabolism | NFATC Transcription Factors | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Osteoclasts - metabolism | Membrane Glycoproteins - genetics | Gene Expression Regulation - drug effects | Proteins - genetics | Carrier Proteins - genetics | TNF Receptor-Associated Factor 6 | Animals | Carrier Proteins - metabolism | Proteins - metabolism | Cell Differentiation - drug effects | Calcineurin - metabolism | Osteoclasts - drug effects | Index Medicus
Journal Article