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Lancet Oncology, The, ISSN 1470-2045, 2012, Volume 13, Issue 8, pp. 782 - 789
Summary Background MEK is a member of the MAPK signalling cascade that is commonly activated in melanoma. Direct inhibition of MEK blocks cell proliferation... 
Hematology, Oncology and Palliative Medicine | SURVIVAL | BRAF | ONCOLOGY | RAF | SOMATIC MUTATIONS | PROGRESSION | Skin Neoplasms - drug therapy | United States | Humans | Middle Aged | Melanoma - enzymology | Male | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - adverse effects | Molecular Targeted Therapy | Uveal Neoplasms - enzymology | Young Adult | Pyridones - administration & dosage | Skin Neoplasms - enzymology | Time Factors | Antineoplastic Agents - adverse effects | DNA Mutational Analysis | Melanoma - genetics | Skin Neoplasms - mortality | Adult | Female | Skin Neoplasms - pathology | MAP Kinase Kinase 1 - antagonists & inhibitors | Uveal Neoplasms - genetics | Uveal Neoplasms - pathology | Drug Administration Schedule | Administration, Oral | Pyrimidinones - adverse effects | Kaplan-Meier Estimate | MAP Kinase Kinase 1 - metabolism | Treatment Outcome | MAP Kinase Kinase 2 - metabolism | Melanoma - pathology | Uveal Neoplasms - drug therapy | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | MAP Kinase Kinase 2 - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Skin Neoplasms - genetics | Uveal Neoplasms - mortality | Aged | Pyrimidinones - administration & dosage | Mutation | Pyridones - adverse effects | Melanoma - mortality | Prevention | Care and treatment | Melanoma | Cancer | Index Medicus
Journal Article
Journal Article
Nature, ISSN 0028-0836, 01/2009, Volume 457, Issue 7229, pp. 599 - 602
BRAF and NRAS are common targets for somatic mutations in benign and malignant neoplasms that arise from melanocytes situated in epithelial structures, and... 
CELLS | ALPHA-SUBUNIT | PATHWAY | MULTIDISCIPLINARY SCIENCES | KINASE-C | BRAF | CANCER | TUMORS | MELANOCYTOSIS | Cell Proliferation | GTP-Binding Protein alpha Subunits - chemistry | Humans | Melanoma - enzymology | Nevus, Blue - pathology | Uveal Neoplasms - enzymology | MAP Kinase Signaling System | Skin Neoplasms - enzymology | Nevus, Blue - genetics | DNA Mutational Analysis | Melanoma - genetics | ras Proteins - chemistry | Melanocytes - pathology | Codon - genetics | Protein Structure, Tertiary | Skin Neoplasms - pathology | Oncogenes - genetics | Uveal Neoplasms - genetics | Melanocytes - enzymology | GTP-Binding Protein alpha Subunits - metabolism | Uveal Neoplasms - pathology | Cells, Cultured | Nevus, Blue - enzymology | GTP-Binding Protein alpha Subunits - genetics | Melanoma - pathology | Mutation - genetics | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Biopsy | Cell Transformation, Neoplastic | Skin Neoplasms - genetics | GTP-Binding Protein alpha Subunits - deficiency | Enzyme Activation | Genes, Dominant - genetics | Apoptosis | Mitogen-Activated Protein Kinases - metabolism | Antibody diversity | Evaluation | Gene mutations | Uvea | Melanoma | Genetic aspects | Research | Health aspects | Cancer | Proteins | Studies | Enzymes | Cell cycle | Mutation | Kinases | Risk factors | Skin cancer | Index Medicus
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2013, Volume 14, Issue 8, pp. 733 - 740
Summary Background Patients with metastatic melanoma, 50% of whose tumours harbour a BRAF mutation, have a poor prognosis. Selumetinib, a MEK1/2 inhibitor, has... 
Hematology, Oncology and Palliative Medicine | CELL LUNG-CANCER | TRIAL | KINASE KINASE-1/2 INHIBITOR | MULTICENTER | ONCOLOGY | ORAL MEK INHIBITOR | IMPROVED SURVIVAL | INHIBITOR AZD6244 ARRY-142886 | OPEN-LABEL | MUTATIONS | VEMURAFENIB | Dacarbazine - adverse effects | Skin Neoplasms - drug therapy | Humans | Middle Aged | Male | Antineoplastic Agents, Alkylating - administration & dosage | Skin Neoplasms - enzymology | Benzimidazoles - administration & dosage | Time Factors | DNA Mutational Analysis | Brazil | Proto-Oncogene Proteins B-raf - metabolism | Dacarbazine - administration & dosage | Genetic Predisposition to Disease | Neoplasms, Unknown Primary - genetics | Europe | Logistic Models | Antineoplastic Agents, Alkylating - therapeutic use | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Protein Kinase Inhibitors - administration & dosage | Phenotype | Mutation | Antineoplastic Agents, Alkylating - adverse effects | Melanoma - mortality | Dacarbazine - therapeutic use | United States | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Melanoma - enzymology | Neoplasms, Unknown Primary - enzymology | Melanoma - genetics | Skin Neoplasms - mortality | Adult | Female | Skin Neoplasms - pathology | Neoplasms, Unknown Primary - drug therapy | Double-Blind Method | Drug Administration Schedule | Kaplan-Meier Estimate | Proportional Hazards Models | Treatment Outcome | Neoplasms, Unknown Primary - mortality | Melanoma - secondary | Disease-Free Survival | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Skin Neoplasms - genetics | Aged | Neoplasms, Unknown Primary - pathology | Care and treatment | Chemotherapy | Gene mutations | Analysis | Melanoma | Metastasis | Cancer | Index Medicus
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 04/2011, Volume 29, Issue 10, pp. 1239 - 1246
Journal Article
Nature, ISSN 0028-0836, 09/2011, Volume 477, Issue 7363, pp. 225 - 228
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 07/2011, Volume 29, Issue 21, pp. 2904 - 2909
Purpose Melanomas harbor aberrations in the c-Kit gene. We tested the efficiency of the tyrosine kinase inhibitor imatinib in selected patients with metastatic... 
ACTIVATION | THERAPY | PROGNOSTIC-FACTORS | EFFICACY | ONCOLOGY | SAFETY | TYROSINE KINASE | CUTANEOUS MELANOMA | MALIGNANT-MELANOMA | GASTROINTESTINAL STROMAL TUMORS | TRENDS | Skin Neoplasms - drug therapy | Exons | United States | Humans | Middle Aged | Melanoma - enzymology | Male | Tomography, X-Ray Computed | Antineoplastic Agents - therapeutic use | Protein Kinase Inhibitors - adverse effects | Proto-Oncogene Proteins c-kit - antagonists & inhibitors | Skin Neoplasms - enzymology | Time Factors | Antineoplastic Agents - adverse effects | Melanoma - genetics | Skin Neoplasms - mortality | China | Adult | Female | Proto-Oncogene Proteins c-kit - genetics | Skin Neoplasms - pathology | Risk Assessment | Risk Factors | Kaplan-Meier Estimate | Survival Rate | Treatment Outcome | Piperazines - therapeutic use | Imatinib Mesylate | Piperazines - adverse effects | Melanoma - secondary | Disease-Free Survival | Gene Amplification | Tumor Burden - drug effects | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Melanoma - drug therapy | Skin Neoplasms - genetics | Pyrimidines - adverse effects | Aged | Benzamides | Mutation | Melanoma - mortality | Imatinib | Toxicity | Melanoma | Clinical trials | Disease control | Protein-tyrosine kinase | Survival | c-Kit protein | Metastases | Tumors | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2014, Volume 124, Issue 12, pp. 5145 - 5158
Patients with gastric and esophageal (GE) adenocarcinoma tumors in which the oncogene ERBB2 has been amplified are routinely treated with a combination of... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | GROWTH-FACTOR RECEPTOR | LUNG-CANCER | GASTRIC-CANCER | TYROSINE KINASE | RESISTANCE | GENOMIC ALTERATIONS | COPY-NUMBER ALTERATION | HER2 | KINASE ACTIVATION | Receptor, Epidermal Growth Factor - genetics | Adenocarcinoma - pathology | Receptor, ErbB-2 - genetics | Humans | Receptor, ErbB-2 - metabolism | Drug Resistance, Neoplasm | Esophageal Neoplasms - diet therapy | Male | Stomach Neoplasms - pathology | Phosphatidylinositol 3-Kinases - metabolism | Antineoplastic Agents - administration & dosage | Esophageal Neoplasms - pathology | Receptor, Epidermal Growth Factor - metabolism | Antibodies, Monoclonal, Humanized - administration & dosage | Biomarkers, Tumor - metabolism | Female | Adenocarcinoma - genetics | Stomach Neoplasms - enzymology | Stomach Neoplasms - genetics | Adenocarcinoma - enzymology | Stomach Neoplasms - drug therapy | Adenocarcinoma - drug therapy | Gene Amplification - drug effects | Phosphatidylinositol 3-Kinases - genetics | Esophageal Neoplasms - enzymology | Esophageal Neoplasms - genetics | Biomarkers, Tumor - genetics | Gene Amplification - genetics | Trastuzumab | Physiological aspects | Genetic aspects | Research | Drug therapy | Esophageal cancer | Oncogenes | Studies | Cloning | Response rates | Breast cancer | Genomes | Kinases | Cancer therapies | Patients | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
The American Journal of Surgical Pathology, ISSN 0147-5185, 03/2016, Volume 40, Issue 3, pp. 368 - 377
Journal Article
The American Journal of Surgical Pathology, ISSN 0147-5185, 11/2015, Volume 39, Issue 11, pp. 1529 - 1539
Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) syndrome is an autosomal dominant syndrome that results from mutations in the fumarate hydratase... 
Fumarate hydratase | Hereditary leiomyomatosis and renal cell carcinoma syndrome (HLRCC) | Uterine smooth muscle tumors | 2sc | SURGERY | 2SC | uterine smooth muscle tumors | HEREDITARY LEIOMYOMATOSIS | PATHOLOGY | FEATURES | INACTIVATION | hereditary leiomyomatosis and renal cell carcinoma syndrome (HLRCC) | fumarate hydratase | FAMILIES | GERMLINE MUTATIONS | SMOOTH-MUSCLE TUMORS | HLRCC SYNDROME | CARCINOMA | FIBROIDS | RENAL-CELL CANCER | Immunohistochemistry | Cysteine - analogs & derivatives | Predictive Value of Tests | Fumarate Hydratase - analysis | Prognosis | Age Factors | Uterine Neoplasms - pathology | Humans | Skin Neoplasms - chemistry | Neoplastic Syndromes, Hereditary | Uterine Neoplasms - enzymology | Young Adult | Skin Neoplasms - enzymology | DNA Mutational Analysis | Leiomyomatosis - diagnosis | Skin Neoplasms - diagnosis | Leiomyomatosis - pathology | Adult | Female | Uterine Neoplasms - diagnosis | Skin Neoplasms - pathology | Uterine Neoplasms - chemistry | Uterine Neoplasms - genetics | Genetic Predisposition to Disease | Biomarkers, Tumor - analysis | Cysteine - analysis | Fumarate Hydratase - genetics | Leiomyomatosis - chemistry | Phenotype | Biopsy | Skin Neoplasms - genetics | Biomarkers, Tumor - genetics | Mutation | Leiomyomatosis - enzymology | Leiomyomatosis - genetics | Index Medicus
Journal Article
Toxicology and Applied Pharmacology, ISSN 0041-008X, 08/2018, Volume 352, pp. 87 - 96
Previously, we proved that caffeic acid (CA), a major dietary phenolic acid, prevents skin carcinogenesis by modulating inflammatory signaling in mouse skin.... 
UV radiation | Photocarcinogenesis | Nucleotide excision repair | Caffeic acid | INDUCED DNA-DAMAGE | ACTIVATION | CELLS IN-VITRO | DIETARY PHYTOCHEMICALS | KINASE | MECHANISMS | CANCER | NUCLEOTIDE EXCISION-REPAIR | FERULIC ACID | PHARMACOLOGY & PHARMACY | TOXICOLOGY | PROGRESSION | Cell Transformation, Neoplastic - radiation effects | Fibroblasts - enzymology | Neoplasms, Radiation-Induced - enzymology | Apoptosis - drug effects | Humans | Neoplasms, Experimental - enzymology | Caffeic Acids - pharmacology | Neoplasms, Experimental - pathology | Skin Neoplasms - enzymology | Skin Neoplasms - prevention & control | DNA Repair Enzymes - metabolism | Neoplasms, Radiation-Induced - prevention & control | Oxidative Stress - radiation effects | Signal Transduction - radiation effects | Neoplasms, Radiation-Induced - pathology | Anticarcinogenic Agents - pharmacology | Skin - pathology | DNA Damage - drug effects | Skin Neoplasms - pathology | DNA Repair - drug effects | Neoplasms, Experimental - prevention & control | PTEN Phosphohydrolase - metabolism | Fibroblasts - pathology | Skin - enzymology | Cell Transformation, Neoplastic - metabolism | Ultraviolet Rays - adverse effects | Animals | Fibroblasts - radiation effects | Signal Transduction - drug effects | Skin - radiation effects | Fibroblasts - drug effects | Mice | Cell Transformation, Neoplastic - drug effects | Oxidative Stress - drug effects | Cell Transformation, Neoplastic - pathology | Skin - drug effects | Proteins | Skin | Cell death | DNA repair | DNA damage | Radiation | Index Medicus
Journal Article
Cancer Research, ISSN 0008-5472, 06/2008, Volume 68, Issue 12, pp. 4541 - 4550
Lysyl oxidase-like 2 (Loxl2) interacts with and stabilizes Snail transcription factor, promoting epithelial-mesenchymal transition. Either Loxl2 or Snail... 
LYSYL OXIDASE | BREAST-CANCER | METASTASIS | TUMOR PROGRESSION | ONCOLOGY | HA-RAS | IN-VIVO | GENE-EXPRESSION | MOLECULAR ROLE | EPITHELIAL-MESENCHYMAL TRANSITIONS | SNAIL | Prognosis | Oligonucleotide Array Sequence Analysis | Tissue Array Analysis | Carcinoma, Squamous Cell - pathology | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Male | Gene Expression Profiling | Amino Acid Oxidoreductases - metabolism | Laryngeal Neoplasms - pathology | Amino Acid Oxidoreductases - genetics | Breast Neoplasms - enzymology | Skin Neoplasms - enzymology | Aged, 80 and over | Biomarkers, Tumor - metabolism | Adult | Female | Laryngeal Neoplasms - enzymology | Retrospective Studies | Snail Family Transcription Factors | Organ Culture Techniques | Skin Neoplasms - pathology | Carcinoma, Squamous Cell - enzymology | Lung Neoplasms - enzymology | RNA, Small Interfering - pharmacology | Amino Acid Oxidoreductases - antagonists & inhibitors | Survival Rate | Transcription Factors - antagonists & inhibitors | Lymphatic Metastasis | Skin Neoplasms - chemically induced | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Transcription Factors - metabolism | Animals | Breast Neoplasms - pathology | Fluorescent Antibody Technique | 9,10-Dimethyl-1,2-benzanthracene | Aged | Mice | Index Medicus
Journal Article