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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
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
Blood, ISSN 1528-0020, 2012, Volume 119, Issue 24, pp. 5795 - 5806
The pathogenesis of hepatosplenic T-cell lymphoma (HSTL), a rare entity mostly derived from γδ T cells and usually with a fatal outcome, remains largely... 
GAMMA-DELTA | TYROSINE KINASE | ALPHA-BETA | NON-HODGKINS-LYMPHOMA | NK-CELL | PI EXPRESSION | RECEPTOR | DRUG-RESISTANCE | HEMATOLOGY | NF-KAPPA-B | CLINICOPATHOLOGICAL ENTITY | Crystallins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Molecular Sequence Data | Male | Receptors, Antigen, T-Cell, gamma-delta - genetics | Gene Expression Profiling | Intracellular Signaling Peptides and Proteins - metabolism | Molecular Targeted Therapy | Young Adult | Base Sequence | Biomarkers, Tumor - metabolism | Adult | Female | Liver Neoplasms - pathology | Membrane Proteins - metabolism | Genes, Neoplasm - genetics | Syk Kinase | Cell Lineage - genetics | Splenic Neoplasms - drug therapy | Liver Neoplasms - genetics | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Splenic Neoplasms - genetics | Liver Neoplasms - drug therapy | Lymphoma, T-Cell - genetics | Receptors, Antigen, T-Cell, alpha-beta - genetics | Isochromosomes - genetics | Drug Resistance, Neoplasm - genetics | Lymphoma, T-Cell - drug therapy | Splenic Neoplasms - pathology | Chromosome Aberrations | Lymphoma, T-Cell - pathology | Aged | Biomarkers, Tumor - genetics | Cluster Analysis | Protein-Tyrosine Kinases - antagonists & inhibitors | pathology | Lymphoma, T-Cell | Genes, Neoplasm | Drug Resistance, Neoplasm | Isochromosomes | Liver Neoplasms | genetics | Crystallins | Receptors, Antigen, T-Cell, alpha-beta | drug therapy | Tumor Markers, Biological | Intracellular Signaling Peptides and Proteins | antagonists & inhibitors | Membrane Proteins | Cell Lineage | Receptors, Antigen, T-Cell, gamma-delta | metabolism | Protein-Tyrosine Kinases | Splenic Neoplasms
Journal Article
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
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
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2017, Volume 355, Issue 6320, pp. 78 - 83
Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting that lineage plasticity facilitates therapeutic resistance... 
PATHWAY | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | SMALL-CELL CARCINOMA | PTEN | GENERATION | TUMORIGENESIS | EXPRESSION | DEFICIENCY | DELETION | EZH2 | Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors | Epigenesis, Genetic | Humans | SOXB1 Transcription Factors - antagonists & inhibitors | Male | Retinoblastoma-Like Protein p107 - genetics | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Neoplasm Metastasis | Prostatic Neoplasms - genetics | SOXB1 Transcription Factors - genetics | Neoplasms, Experimental - genetics | Adenocarcinoma - genetics | Prostatic Neoplasms - drug therapy | Neuroendocrine Tumors - pathology | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Enhancer of Zeste Homolog 2 Protein - genetics | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Neuroendocrine Tumors - genetics | Cell Lineage | Drug Resistance, Neoplasm - genetics | Animals | Androgen Antagonists - therapeutic use | Cell Line, Tumor | Neuroendocrine Tumors - drug therapy | Cell Plasticity | Mice | Mutation | Neoplasms, Experimental - drug therapy | Prevention | Antimitotic agents | Epigenetic inheritance | Development and progression | Genetic aspects | Dosage and administration | Metastasis | Gene expression | Antineoplastic agents | Drug resistance | Health aspects | Prostate cancer | Drugs | Therapy | Deprivation | Histology | Hormones | Suppressors | Switching | Signal transduction | Sensitivity | Androgens | Inhibitors | Rodents | Plasticity | Epigenetics | Tumor suppressor genes | Plastic properties | Prostate | Cancer | Tumors | Mutations
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
by Abbosh, Christopher and Birkbak, Nicolai J and Wilson, Gareth A and Jamal-Hanjani, Mariam and Constantin, Tudor and Salari, Raheleh and Le Quesne, John and Moore, David A and Veeriah, Selvaraju and Rosenthal, Rachel and Marafioti, Teresa and Kirkizlar, Eser and Watkins, Thomas B. K and McGranahan, Nicholas and Ward, Sophia and Martinson, Luke and Riley, Joan and Fraioli, Francesco and Al Bakir, Maise and Grönroos, Eva and Zambrana, Francisco and Endozo, Raymondo and Bi, Wenya Linda and Fennessy, Fiona M and Sponer, Nicole and Johnson, Diana and Laycock, Joanne and Shafi, Seema and Czyzewska-Khan, Justyna and Rowan, Andrew and Chambers, Tim and Matthews, Nik and Turajlic, Samra and Hiley, Crispin and Lee, Siow Ming and Forster, Martin D and Ahmad, Tanya and Falzon, Mary and Borg, Elaine and Lawrence, David and Hayward, Martin and Kolvekar, Shyam and Panagiotopoulos, Nikolaos and Janes, Sam M and Thakrar, Ricky and Ahmed, Asia and Blackhall, Fiona and Summers, Yvonne and Hafez, Dina and Naik, Ashwini and Ganguly, Apratim and Kareht, Stephanie and Shah, Rajesh and Joseph, Leena and Marie Quinn, Anne and Crosbie, Phil A and Naidu, Babu and Middleton, Gary and Langman, Gerald and Trotter, Simon and Nicolson, Marianne and Remmen, Hardy and Kerr, Keith and Chetty, Mahendran and Gomersall, Lesley and Fennell, Dean A and Nakas, Apostolos and Rathinam, Sridhar and Anand, Girija and Khan, Sajid and Russell, Peter and Ezhil, Veni and Ismail, Babikir and Irvin-Sellers, Melanie and Prakash, Vineet and Lester, Jason F and Kornaszewska, Malgorzata and Attanoos, Richard and Adams, Haydn and Davies, Helen and Oukrif, Dahmane and Akarca, Ayse U and Hartley, John A and