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Nature (London), ISSN 1476-4687, 2013, Volume 497, Issue 7447, pp. 108 - 112
Cancers acquire resistance to systemic treatment as a result of clonal evolution and selection(1,2... 
HETEROGENEITY | LUNG-CANCER | ACTIVATION | EVOLUTION | VARIANTS | AXL | MULTIDISCIPLINARY SCIENCES | TAMOXIFEN RESISTANCE | TUMOR-CELLS | MUTATIONS | Lung Neoplasms - drug therapy | Genomics | Humans | ErbB Receptors - genetics | 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
Journal Article
Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
.... To understand the resistance mechanisms, we conducted whole-genome CRISPR-Cas9 synthetic-viability/resistance screens in BRCA1-deficient breast cancer cells treated with PARP inhibitors... 
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 | Polymerase | 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
Journal of Thoracic Oncology, ISSN 1556-0864, 03/2013, Volume 8, Issue 3, pp. 346 - 351
Journal Article
Seminars in Oncology, ISSN 0093-7754, 2015, Volume 42, Issue 6, pp. 801 - 819
.... Most of these molecular alterations promote multiple steps of carcinogenesis in FGFR oncogene-addicted cells, increasing cell proliferation, angiogenesis, and drug resistance... 
BREAST-CANCER | LUNG-CANCER | IN-VITRO | ONCOLOGY | SQUAMOUS-CELL CARCINOMA | RESISTANCE | GENE AMPLIFICATION | POTENTIAL THERAPEUTIC TARGET | PROGNOSTIC-SIGNIFICANCE | ANTITUMOR-ACTIVITY | EXPRESSION | Neoplasms - metabolism | Gastrointestinal Neoplasms - genetics | Gastrointestinal Neoplasms - drug therapy | Humans | Brain Neoplasms - pathology | Fibroblast Growth Factors - genetics | Brain Neoplasms - metabolism | Head and Neck Neoplasms - metabolism | Breast Neoplasms - metabolism | Fibroblast Growth Factors - metabolism | Gastrointestinal Neoplasms - pathology | Glioblastoma - genetics | Receptors, Fibroblast Growth Factor - genetics | Female | Glioblastoma - metabolism | Antineoplastic Agents - pharmacology | Molecular Targeted Therapy - methods | Gastrointestinal Neoplasms - metabolism | Biomarkers, Tumor - analysis | Head and Neck Neoplasms - drug therapy | Receptors, Fibroblast Growth Factor - antagonists & inhibitors | Thoracic Neoplasms - pathology | Brain Neoplasms - genetics | Brain Neoplasms - drug therapy | Breast Neoplasms - drug therapy | Thoracic Neoplasms - metabolism | Head and Neck Neoplasms - pathology | Neoplasms - drug therapy | Breast Neoplasms - genetics | Thoracic Neoplasms - genetics | Breast Neoplasms - pathology | Glioblastoma - pathology | Receptors, Fibroblast Growth Factor - metabolism | Head and Neck Neoplasms - genetics | Fibroblast Growth Factors - antagonists & inhibitors | Thoracic Neoplasms - drug therapy | Glioblastoma - drug therapy | Neoplasms - pathology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Index Medicus
Journal Article
Journal Article
The lancet oncology, ISSN 1470-2045, 2017, 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 | POLY(ADP-RIBOSE) POLYMERASE | OLAPARIB | ONCOLOGY | HOMOLOGOUS RECOMBINATION DEFICIENCY | MUTANT-CELLS | DNA-REPAIR | CANCER | HETEROZYGOSITY | TUMORS | BREAST | 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
Journal Article
Nature (London), ISSN 1476-4687, 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
Journal Article
Cancer chemotherapy and pharmacology, ISSN 1432-0843, 2019, Volume 84, Issue 3, pp. 487 - 499
... in breast, prostate, lung, endometrial, and ovarian tumors: relevance for resistance to taxanes Maarten van Eijk 1 · René J. Boosman 1 · Alfred H. Schinkel 2 · Alwin D... 
Intratumoral | Ritonavir | Paclitaxel | Docetaxel | CYP | Review | Journal Article | Medicine & Public Health | Oncology | Cancer Research | Pharmacology/Toxicology | PREGNANE-X RECEPTOR | IMMUNOHISTOCHEMICAL LOCALIZATION | DOCETAXEL RESISTANCE | CYP3A4 EXPRESSION | TARGETED THERAPIES | MESSENGER-RNA | ONCOLOGY | P450-MEDIATED METABOLISM | BIOLOGICAL-ACTIVITY | PHARMACOLOGY & PHARMACY | HIV-1 PROTEASE INHIBITOR | METABOLIZING-ENZYMES | Lung Neoplasms - drug therapy | Taxoids - pharmacology | Humans | Ovarian Neoplasms - pathology | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | Male | Breast Neoplasms - enzymology | Female | Antineoplastic Agents - pharmacology | Cytochrome P-450 CYP2C8 - metabolism | Ovarian Neoplasms - drug therapy | Prostatic Neoplasms - drug therapy | Prostatic Neoplasms - pathology | Endometrial Neoplasms - enzymology | Lung Neoplasms - enzymology | Neoplasms - enzymology | Breast Neoplasms - drug therapy | Ovarian Neoplasms - enzymology | Neoplasms - drug therapy | Breast Neoplasms - pathology | Cytochrome P-450 CYP3A - metabolism | Prostatic Neoplasms - enzymology | Endometrial Neoplasms - drug therapy | Endometrial Neoplasms - pathology | Neoplasms - pathology | Antimitotic agents | Protease inhibitors | Proteases | Pharmacy | Cytochrome P-450 | Physiological aspects | Drugstores | Antineoplastic agents | Ovarian cancer | Cytochrome | Enzymes | Cytochrome P450 | Proteinase inhibitors | Taxane | Metabolism | Anticancer properties | Antitumor agents | Lungs | Drug metabolism | Breast | Solid tumors | Taxanes | Prostate | Endometrium | Tumors | Cytochromes P450
Journal Article
The Journal of clinical investigation, ISSN 1558-8238, 2018, Volume 128, Issue 6, pp. 2500 - 2518
Although aberrant ECFR signaling is widespread in cancer, EGFR inhibition is effective only in a subset of non-small cell lung cancer (NSCLC) with EGFR... 
TARGETED THERAPY | MEDICINE, RESEARCH & EXPERIMENTAL | GROWTH-FACTOR RECEPTOR | TUMOR-NECROSIS-FACTOR | ACQUIRED-RESISTANCE | TYROSINE KINASE INHIBITOR | NEVER-SMOKERS | NF-KAPPA-B | FACTOR-ALPHA | SIGNALING NETWORKS | TKI RESISTANCE | Tumor Necrosis Factor-alpha - metabolism | Humans | Lung Neoplasms - metabolism | Tumor Necrosis Factor-alpha - genetics | ErbB Receptors - genetics | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | MicroRNAs - metabolism | Neoplasm Proteins - antagonists & inhibitors | Neoplasm Proteins - metabolism | RNA, Messenger - metabolism | RNA, Neoplasm - metabolism | Neoplasms, Experimental - pathology | Neoplasms, Experimental - genetics | Female | Neoplasm Proteins - genetics | Lung Neoplasms - genetics | A549 Cells | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Carcinoma, Non-Small-Cell Lung - genetics | RNA, Messenger - genetics | Neoplasms, Experimental - therapy | Lung Neoplasms - therapy | Carcinoma, Non-Small-Cell Lung - therapy | Animals | Mice, Nude | RNA, Neoplasm - genetics | Mice | MicroRNAs - genetics | Neoplasms, Experimental - metabolism | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Care and treatment | Gene mutations | Tumor necrosis factor | Genetic aspects | Cellular signal transduction | Research | Genetic transcription | Lung cancer, Non-small cell | NF-κB protein | Epidermal growth factor receptors | Transcription | Lung cancer | Non-small cell lung carcinoma | Gene expression | Kinases | Patients | Proteins | Epidermal growth factor | Medical prognosis | MicroRNAs | Xenografts | Tumor necrosis factor-TNF | Ligands | Mutation | mRNA stability
Journal Article