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Nature, ISSN 0028-0836, 11/2015, Volume 527, Issue 7579, pp. 472 - 476
The role of epithelial-to-mesenchymal transition (EMT) in metastasis is a longstanding source of debate, largely owing to an inability to monitor transient and... 
CANCER-CELLS | STEM-CELLS | THERAPY | MULTIDISCIPLINARY SCIENCES | RESISTANCE | INDUCTION | MODEL | MIR-200 FAMILY | EXPRESSION | BREAST | PLASTICITY | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Antineoplastic Agents, Alkylating - pharmacology | Epithelial-Mesenchymal Transition - drug effects | Lung Neoplasms - pathology | Male | Epithelial-Mesenchymal Transition - genetics | Cyclophosphamide - therapeutic use | Mammary Neoplasms, Experimental - genetics | Cell Tracking | Lung Neoplasms - secondary | Neoplasm Metastasis - drug therapy | Mammary Neoplasms, Experimental - pathology | Female | Disease Models, Animal | Mammary Neoplasms, Experimental - drug therapy | Lung Neoplasms - genetics | Reproducibility of Results | Disease Progression | Antineoplastic Agents, Alkylating - therapeutic use | Cell Lineage | Neoplasm Metastasis - genetics | Drug Resistance, Neoplasm - genetics | Animals | Neoplasm Metastasis - pathology | Cyclophosphamide - pharmacology | Cell Proliferation - drug effects | Mice | MicroRNAs - genetics | Drug Resistance, Neoplasm - drug effects | Development and progression | Metastasis | Drug resistance | Cell differentiation | Health aspects | Lung cancer | Chemotherapy | Analysis | Stem cells | Cancer | Studies | Genotype & phenotype | Transgenic animals | Rodents | Morphology | Fibroblasts | Breast cancer | Cancer therapies | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2013, Volume 497, Issue 7447, pp. 108 - 112
Cancers acquire resistance to systemic treatment as a result of clonal evolution and selection(1,2). Repeat biopsies to study genomic evolution as a result of... 
HETEROGENEITY | LUNG-CANCER | ACTIVATION | EVOLUTION | VARIANTS | AXL | MULTIDISCIPLINARY SCIENCES | TAMOXIFEN RESISTANCE | TUMOR-CELLS | MUTATIONS | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Genomics | Humans | Ovarian Neoplasms - pathology | Lung Neoplasms - pathology | Antineoplastic Agents - therapeutic use | Ovarian Neoplasms - genetics | Neoplasms - genetics | DNA Mutational Analysis | Female | Antineoplastic Agents - pharmacology | DNA, Neoplasm - analysis | Ovarian Neoplasms - drug therapy | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Intercellular Signaling Peptides and Proteins - genetics | Breast Neoplasms - drug therapy | Genome, Human - genetics | Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Exome - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Breast Neoplasms - pathology | Retinoblastoma Protein - genetics | Plasma - chemistry | Alleles | Carcinoma, Non-Small-Cell Lung - drug therapy | DNA, Neoplasm - genetics | Neoplasms - pathology | Mediator Complex Subunit 1 - genetics | Drug Resistance, Neoplasm - drug effects | Evolution, Molecular | Antimitotic agents | Care and treatment | Physiological aspects | Dosage and administration | Genetic aspects | Research | Nucleotide sequencing | Drug resistance | Antineoplastic agents | DNA sequencing | Blood plasma | Cancer | Plasma | Biopsy | Breast cancer | Genomes | Mutation | Patients | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Nature Communications, ISSN 2041-1723, 03/2016, Volume 7, Issue 1, pp. 11150 - 11150
Journal Article
Nature, ISSN 0028-0836, 04/2015, Volume 520, Issue 7547, pp. 368 - 372
Drug resistance invariably limits the clinical efficacy of targeted therapy with kinase inhibitors against cancer(1,2). Here we show that targeted therapy with... 
CNS CELL-TYPES | MELANOMA | METASTASIS | MICROENVIRONMENT | TRANSLATIONAL PROFILING APPROACH | MULTIDISCIPLINARY SCIENCES | RAF INHIBITOR RESISTANCE | ACQUIRED-RESISTANCE | KINASE INHIBITORS | DRUG-RESISTANCE | CANCER CHEMORESISTANCE | Lung Neoplasms - drug therapy | Adenocarcinoma - pathology | Clone Cells - drug effects | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Proto-Oncogene Proteins c-fos - deficiency | Adenocarcinoma - metabolism | Neoplasm Metastasis - drug therapy | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Proto-Oncogene Proteins c-akt - metabolism | Melanoma - metabolism | Tumor Microenvironment - drug effects | Cell Survival - drug effects | Melanoma - pathology | Down-Regulation - drug effects | Enzyme Activation - drug effects | Adenocarcinoma - drug therapy | Disease Progression | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Cell Movement - drug effects | Lung Neoplasms - secretion | Melanoma - secretion | Animals | Clone Cells - pathology | Metabolome - drug effects | Signal Transduction - drug effects | Neoplasm Metastasis - pathology | Protein Kinase Inhibitors - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Adenocarcinoma - secretion | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Pharmaceutical research | Care and treatment | Oncology, Experimental | Dosage and administration | Research | Drug therapy | Drug resistance | Antineoplastic agents | Tumors | Cancer | Melanoma | Mutation | Metastasis | Kinases | Cancer therapies | Index Medicus
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 12/2015, Volume 33, Issue 34, pp. 4015 - 4022
Journal Article
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
Lancet Oncology, The, ISSN 1470-2045, 2016, Volume 18, Issue 1, pp. 75 - 87
Summary Background Poly(ADP-ribose) polymerase (PARP) inhibitors have activity in ovarian carcinomas with homologous recombination deficiency. Along with BRCA1... 
Hematology, Oncology and Palliative Medicine | BRCA MUTATION | POLY(ADP-RIBOSE) POLYMERASE | RANDOMIZED PHASE-2 | ONCOLOGY | HOMOLOGOUS RECOMBINATION DEFICIENCY | MUTANT-CELLS | PROSTATE-CANCER | INHIBITORS | DNA-REPAIR | NEGATIVE BREAST-CANCER | GENOMIC LOSS | Prognosis | Prospective Studies | Follow-Up Studies | Humans | Middle Aged | Ovarian Neoplasms - pathology | Salvage Therapy | Neoplasm Recurrence, Local - drug therapy | Germ-Line Mutation - genetics | Neoplasm Recurrence, Local - pathology | Ovarian Neoplasms - genetics | Neoplasms, Glandular and Epithelial - genetics | Peritoneal Neoplasms - drug therapy | Fallopian Tube Neoplasms - genetics | Female | Antineoplastic Agents - pharmacology | Poly(ADP-ribose) Polymerases - chemistry | Ovarian Neoplasms - drug therapy | Platinum - pharmacology | Fallopian Tube Neoplasms - drug therapy | Peritoneal Neoplasms - pathology | Neoplasms, Glandular and Epithelial - pathology | Fallopian Tube Neoplasms - pathology | Survival Rate | Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use | BRCA1 Protein - genetics | International Agencies | Peritoneal Neoplasms - genetics | Neoplasms, Glandular and Epithelial - drug therapy | Carcinoma, Ovarian Epithelial | Indoles - therapeutic use | Neoplasm Recurrence, Local - genetics | Aged | Neoplasm Staging | BRCA2 Protein - genetics | Drug Resistance, Neoplasm - drug effects | Sugars | Monosaccharides | Ovarian cancer | Analysis | Carcinoma | Cancer | Index Medicus
Journal Article