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Nature reviews. Cancer, ISSN 1474-1768, 2017, Volume 17, Issue 2, pp. 93 - 115
Journal Article
Cancer discovery, ISSN 2159-8290, 2017, Volume 7, Issue 4, pp. 400 - 409
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies in patients with advanced or... 
REARRANGEMENT | ONCOGENE | ONCOLOGY | ANALOG SECRETORY CARCINOMA | LANDSCAPE | KINASE FUSIONS | SARCOMAS | ETV6-NTRK3 GENE FUSION | CRIZOTINIB | GENOMIC ALTERATIONS | CLINICAL-RESPONSE | Benzamides - pharmacokinetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Receptor, trkA - antagonists & inhibitors | Male | Receptor, trkB - genetics | Indazoles - administration & dosage | Protein Kinase Inhibitors - adverse effects | Mammary Analogue Secretory Carcinoma - genetics | Dose-Response Relationship, Drug | Benzamides - administration & dosage | Membrane Glycoproteins - antagonists & inhibitors | Receptor, trkC - genetics | Anaplastic Lymphoma Kinase | Melanoma - genetics | Colorectal Neoplasms - drug therapy | Receptor, trkB - antagonists & inhibitors | Aged, 80 and over | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Benzamides - adverse effects | Carcinoma, Non-Small-Cell Lung - pathology | Crizotinib | Protein Kinase Inhibitors - pharmacokinetics | Proto-Oncogene Proteins - antagonists & inhibitors | Pyridines - administration & dosage | Carcinoma, Non-Small-Cell Lung - genetics | Receptor, trkC - antagonists & inhibitors | Melanoma - pathology | Mammary Analogue Secretory Carcinoma - drug therapy | Membrane Glycoproteins - genetics | Protein Kinase Inhibitors - administration & dosage | Sequestosome-1 Protein - genetics | Pyrazoles - administration & dosage | Indazoles - pharmacokinetics | Receptor Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - genetics | Melanoma - drug therapy | Adolescent | Receptor, trkA - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Indazoles - adverse effects | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 32, pp. 4635 - 4647
...). APBs are PML bodies containing telomeric DNA and telomere-binding proteins, and are observed only in a small fraction of cells within asynchronously dividing ALT-positive cell populations... 
Telomeres | siRNA | Alternative lengthening of telomeres | Methionine restriction | PML | ALT-associated PML bodies | CANCER-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | telomeres | DNA-DAMAGE | MAMMALIAN-CELLS | PROTEIN COMPLEX | CELL BIOLOGY | HUMAN RAP1 | METABOLIC DEFECT | LARGE-BODY FORMATION | NUCLEAR-BODIES | ONCOLOGY | alternative lengthening of telomeres | methionine restriction | GENETICS & HEREDITY | PROMYELOCYTIC LEUKEMIA BODIES | TUMOR-CELL-LINES | Humans | Neoplasm Proteins - antagonists & inhibitors | Resting Phase, Cell Cycle | Autoantigens - genetics | RNA Interference | Neoplasm Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Telomeric Repeat Binding Protein 2 - antagonists & inhibitors | DNA Repair Enzymes - physiology | DNA-Binding Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - physiology | Genetic Techniques | Autoantigens - physiology | Tumor Suppressor Proteins - physiology | G1 Phase | Cell Line, Tumor | Intracellular Signaling Peptides and Proteins - physiology | Cell Cycle Proteins - physiology | Telomeric Repeat Binding Protein 1 - physiology | Tumor Suppressor Proteins - antagonists & inhibitors | Neoplasm Proteins - physiology | DNA Repair Enzymes - genetics | Telomeric Repeat Binding Protein 1 - genetics | Cell Cycle Proteins - antagonists & inhibitors | MRE11 Homologue Protein | Telomere-Binding Proteins - genetics | Tumor Suppressor Proteins - genetics | Telomere-Binding Proteins - physiology | Cell Cycle Proteins - genetics | Telomere - metabolism | DNA Repair Enzymes - antagonists & inhibitors | Nuclear Proteins - genetics | Methionine - deficiency | Telomere - genetics | Transcription Factors - physiology | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | RNA, Small Interfering - pharmacology | Antigens, Nuclear - physiology | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Telomere-Binding Proteins - antagonists & inhibitors | Antigens, Nuclear - genetics | Nuclear Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 1 - antagonists & inhibitors | Cell Proliferation - drug effects | Nuclear Proteins - physiology | Telomeric Repeat Binding Protein 2 - genetics | Tumor Suppressor p53-Binding Protein 1 | Promyelocytic Leukemia Protein | Physiological aspects | Genetic aspects | Research | Cancer cells | Proteins | Ribonucleic acid | Cell cycle | Genetics | Oncology | Ribonucleic acid--RNA | DNA repair | Cancer
Journal Article
Cell reports (Cambridge), ISSN 2211-1247, 2015, Volume 12, Issue 12, pp. 1968 - 1977
Breast cancers (BCs) typically express estrogen receptors (ERs) but frequently exhibit de novo or acquired resistance to hormonal therapies. Here, we show that... 
NOTCH | ESTROGEN | ADJUVANT TAMOXIFEN | RECEPTOR | CELL BIOLOGY | Estradiol - analogs & derivatives | Receptors, Estrogen - metabolism | Neoplastic Stem Cells - drug effects | Receptors, Notch - metabolism | Homeodomain Proteins - metabolism | Humans | Retinal Dehydrogenase - metabolism | p-Aminoazobenzene - analogs & derivatives | Receptors, Notch - genetics | Fulvestrant | Receptors, Notch - antagonists & inhibitors | Basic Helix-Loop-Helix Transcription Factors - metabolism | Neoplastic Stem Cells - metabolism | Serrate-Jagged Proteins | p-Aminoazobenzene - pharmacology | Neoplastic Stem Cells - pathology | Estradiol - pharmacology | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Signal Transduction | Isoenzymes - genetics | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | Benzazepines - pharmacology | Retinal Dehydrogenase - genetics | Breast Neoplasms - drug therapy | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Survival Analysis | Cell Line, Tumor | Retinal Dehydrogenase - antagonists & inhibitors | Mice | Calcium-Binding Proteins - genetics | Transcription Factor HES-1 | Gene Expression Regulation, Neoplastic | Cell Cycle Proteins - antagonists & inhibitors | Estrogen Receptor Antagonists - pharmacology | Intercellular Signaling Peptides and Proteins - metabolism | Isoenzymes - metabolism | Cell Cycle Proteins - genetics | Female | Membrane Proteins - metabolism | Calcium-Binding Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Receptors, Estrogen - genetics | Antineoplastic Agents, Hormonal - pharmacology | Intercellular Signaling Peptides and Proteins - genetics | Proto-Oncogene Proteins - genetics | Basic Helix-Loop-Helix Transcription Factors - antagonists & inhibitors | Aldehyde Dehydrogenase 1 | Homeodomain Proteins - genetics | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - pathology | Homeodomain Proteins - antagonists & inhibitors | Tamoxifen - pharmacology | Breast Neoplasms - mortality | Cell Proliferation - drug effects | Isoenzymes - antagonists & inhibitors | Receptor, Notch4 | Drug Resistance, Neoplasm - drug effects | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Cancer and Oncology | Medicin och hälsovetenskap | Cancer och onkologi
Journal Article
Nature medicine, ISSN 1546-170X, 2012, Volume 18, Issue 8, pp. 1239 - 1247
... (encoding tumor protein 53) is a common step in human cancer. However, in melanoma-A highly chemotherapy-resistant disease-TP53 mutations are rare, raising... 
MEDICINE, RESEARCH & EXPERIMENTAL | N-RAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR ACTIVITY | STAPLED P53 | BRAF | MALIGNANT-MELANOMA | P53 PATHWAY | CELL-DEATH | CELL BIOLOGY | BREAST-CANCER | METASTATIC MELANOMA | IN-VIVO | Up-Regulation | Proto-Oncogene Proteins c-mdm2 - genetics | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Recombinant Fusion Proteins - physiology | Skin Neoplasms - chemistry | Male | Melanocytes - metabolism | Neoplasm Proteins - antagonists & inhibitors | Cell Line, Tumor - transplantation | Proto-Oncogene Proteins - biosynthesis | Tumor Suppressor Protein p53 - physiology | Cell-Penetrating Peptides - pharmacology | Nuclear Proteins - biosynthesis | Female | Antineoplastic Agents - pharmacology | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line, Tumor - metabolism | Melanoma - chemistry | Proto-Oncogene Proteins c-mdm2 - biosynthesis | Proto-Oncogene Proteins - antagonists & inhibitors | Tumor Stem Cell Assay | Membrane Proteins - genetics | Neoplasm Proteins - biosynthesis | Melanoma, Experimental - etiology | Mice, Inbred C57BL | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Melanoma - pathology | Melanoma - secondary | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Melanoma, Experimental - genetics | GTP Phosphohydrolases - genetics | Keratinocytes - metabolism | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Signal Transduction - physiology | Mice | Nuclear Proteins - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Care and treatment | Gene mutations | Melanoma | Diagnosis | Research | Gene expression | Identification and classification | Skin cancer | Proteins | Cell growth | Mutation | Cell cycle
Journal Article
Cancer cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer
Journal Article