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Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7387, pp. 100 - 104
Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma(1). However, colon... 
PANITUMUMAB | TARGET | CETUXIMAB | MELANOMA | BRAF MUTATIONS | MULTIDISCIPLINARY SCIENCES | PAPILLARY THYROID-CARCINOMA | KRAS | METASTATIC COLORECTAL-CANCER | Erlotinib Hydrochloride | Receptor, Epidermal Growth Factor - agonists | Apoptosis - drug effects | Colorectal Neoplasms - genetics | Humans | Antineoplastic Agents - therapeutic use | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | RNA Interference | Colorectal Neoplasms - drug therapy | HEK293 Cells | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Cetuximab | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Colorectal Neoplasms - enzymology | Antibodies, Monoclonal - pharmacology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Drug Synergism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Quinazolines - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Feedback, Physiological - drug effects | Indoles - therapeutic use | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Colorectal Neoplasms - pathology | Quinazolines - pharmacology | Drug Resistance, Neoplasm - drug effects | Proteins | Library collections | Studies | Phosphorylation | Kinases | Tumors | Index Medicus
Journal Article
Methods in Molecular Biology, ISSN 1064-3745, 2016, Volume 1470, pp. 49 - 73
Functional genomic screens using shRNA technology are a great tool in biomedical research. As more labs gain access to the necessary reagents and technology to... 
RNAi | Functional genetics | shRNA | Screens | Mammals - genetics | Cell Line | RNA, Small Interfering - genetics | Transduction, Genetic | Gene Library | Humans | Workflow | RNA, Small Interfering - analysis | Polymerase Chain Reaction - methods | Animals | Lentivirus - genetics | Genomics - methods | High-Throughput Nucleotide Sequencing - methods | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 508, Issue 1, pp. 118 - 122
Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably(1,2).... 
GROWTH-FACTOR RECEPTOR | BRAF INHIBITOR | RAF INHIBITION | CELLS | MULTIDISCIPLINARY SCIENCES | IMPROVED SURVIVAL | DIFFERENTIATION | C-JUN | CANCER | EXPRESSION | EGFR | Receptor, Epidermal Growth Factor - genetics | Humans | Receptor Protein-Tyrosine Kinases - biosynthesis | Cellular Senescence - drug effects | Melanoma - enzymology | Antineoplastic Agents - administration & dosage | Receptor, Platelet-Derived Growth Factor beta - genetics | Indoles - administration & dosage | Mitogen-Activated Protein Kinase Kinases - metabolism | Receptor, Epidermal Growth Factor - metabolism | Flow Cytometry | Melanoma - genetics | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Proto-Oncogene Proteins B-raf - metabolism | Receptor, Platelet-Derived Growth Factor beta - metabolism | Receptor, Epidermal Growth Factor - biosynthesis | Gene Library | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Protein Kinase Inhibitors - administration & dosage | Transforming Growth Factor beta - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Transforming Growth Factor beta - metabolism | Receptor, Platelet-Derived Growth Factor beta - biosynthesis | Sulfonamides - administration & dosage | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Proteins | Biopsy | Rodents | Genes | Melanoma | Mutation | Kinases | Drug resistance | Patients | Tumors | Index Medicus
Journal Article
Cancer Research, ISSN 0008-5472, 11/2008, Volume 68, Issue 22, pp. 9221 - 9230
Journal Article
Cancer Cell, ISSN 1535-6108, 10/2007, Volume 12, Issue 4, pp. 395 - 402
A large-scale RNA interference screen to discover genes involved in trastuzumab resistance in breast cancer identified only as a modulator of drug sensitivity.... 
CELLCYCLE | CELLS | OVEREXPRESSION | PIK3CA MUTATIONS | INHIBITION | EFFICACY | ONCOLOGY | HERCEPTIN | MONOCLONAL-ANTIBODY | RECEPTORS | CHEMOTHERAPY | P53 | Oligonucleotide Array Sequence Analysis | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Antibodies, Monoclonal - therapeutic use | Antineoplastic Agents - therapeutic use | Phosphatidylinositol 3-Kinases - metabolism | Breast Neoplasms - metabolism | Patient Selection | Antibodies, Monoclonal, Humanized | Breast Neoplasms - enzymology | RNA Interference | Biomarkers, Tumor - metabolism | Adult | Female | Antineoplastic Agents - pharmacology | Receptor, ErbB-2 - antagonists & inhibitors | PTEN Phosphohydrolase - genetics | Transduction, Genetic | Antibodies, Monoclonal - pharmacology | Kaplan-Meier Estimate | PTEN Phosphohydrolase - metabolism | Gene Expression Profiling - methods | Treatment Outcome | Signal Transduction - genetics | Breast Neoplasms - drug therapy | Disease Progression | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Signal Transduction - drug effects | Cell Line, Tumor | Breast Neoplasms - mortality | Aged | Biomarkers, Tumor - genetics | Mutation | Trastuzumab | Cohort Studies | RNA, Small Interfering - metabolism | Index Medicus
Journal Article
Gut, ISSN 0017-5749, 9/2019
ObjectivesHepatocellular carcinoma (HCC) is one of the most frequent malignancies and a major leading cause of cancer-related deaths worldwide. Several... 
Journal Article
Cell Reports, ISSN 2211-1247, 10/2014, Volume 7, Issue 1, pp. 86 - 93
Journal Article
Cancer Research, ISSN 0008-5472, 11/2015, Volume 75, Issue 22 Supplement 2, pp. B2 - B2-37
Journal Article
Cancer Research, ISSN 0008-5472, 06/2019, Volume 79, Issue 11, pp. 2933 - 2946
Although many patients with colorectal cancer initially respond to the chemotherapeutic agent oxaliplatin, acquired resistance to this treatment remains a... 
Journal Article
Cell Reports, ISSN 2211-1247, 09/2015, Volume 12, Issue 12, pp. 1978 - 1985
Most ( ) mutant melanomas are sensitive to selective BRAF inhibitors, but mutant colon cancers are intrinsically resistant to these drugs because of feedback... 
COLON-CANCER | SHP2 PTPN11 | LUNG-CANCER | MEK INHIBITION | BRAF(V600E) INHIBITION | GROWTH | PROTEIN-TYROSINE PHOSPHATASES | RAF INHIBITORS | MUTATIONS | NOONAN-SYNDROME | CELL BIOLOGY | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | RNA, Small Interfering - genetics | Receptor, Epidermal Growth Factor - genetics | ras Proteins - genetics | Colonic Neoplasms - genetics | Colonic Neoplasms - drug therapy | Humans | Gene Expression Regulation, Neoplastic | Genomic Library | ras Proteins - metabolism | Colonic Neoplasms - metabolism | MAP Kinase Signaling System | Receptor, Epidermal Growth Factor - metabolism | Melanoma - genetics | Indoles - pharmacology | Lentivirus - genetics | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Melanoma - metabolism | Transduction, Genetic | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - antagonists & inhibitors | Melanoma - pathology | Sulfonamides - pharmacology | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Proto-Oncogene Proteins B-raf - genetics | Colonic Neoplasms - pathology | Melanoma - drug therapy | Cell Line, Tumor | Mice, Inbred NOD | High-Throughput Nucleotide Sequencing | Mice | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Genetic Vectors | Drug Resistance, Neoplasm - drug effects | RNA, Small Interfering - metabolism | Index Medicus
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 12/2018, Volume 215, Issue 12, pp. 3115 - 3135
Kras-driven non-small-cell lung cancers (NSCLCs) are a leading cause of death with limited therapeutic options. Many NSCLCs exhibit high levels of Ezh2, the... 
GROUP GENE EZH2 | MEDICINE, RESEARCH & EXPERIMENTAL | PATHWAY | MOUSE MODEL | RESISTANCE | IMMUNOLOGY | CELL | EXPRESSION | PROGRESSION | REPRESSIVE COMPLEX 2 | RNAI SCREEN | Index Medicus | 307 | 311
Journal Article