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Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 3846 - 3856
Persistently activated or tyrosine-phosphorylated STAT3 (pSTAT3) is found in 50% of lung adenocarcinomas. pSTAT3 is found in primary adenocarcinomas and cell... 
RECEPTOR GENE-MUTATIONS | BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | SIGNALING PATHWAYS | CONSTITUTIVE ACTIVATION | EPIDERMAL-GROWTH-FACTOR | PROSTATE-CANCER CELLS | SQUAMOUS-CELL CARCINOMA | TYROSINE KINASES | NF-KAPPA-B | MAMMARY EPITHELIAL-CELLS | Janus Kinases | Neoplasm Transplantation | Receptor, Epidermal Growth Factor - genetics | Transcription, Genetic - drug effects | Adenocarcinoma - pathology | Interleukin-6 - antagonists & inhibitors | Cytokine Receptor gp130 - genetics | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Receptor, Epidermal Growth Factor - metabolism | Adenocarcinoma - metabolism | Female | Adenocarcinoma - genetics | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Gene Expression Regulation, Neoplastic - genetics | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Lung Neoplasms - genetics | Cytokine Receptor gp130 - metabolism | Interleukin-6 - genetics | RNA, Small Interfering - pharmacology | Enzyme Inhibitors - pharmacology | Lung Neoplasms - therapy | Signal Transduction - genetics | Animals | Adenocarcinoma - therapy | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Interleukin-6 - biosynthesis | Mice | Mutation | Transcription, Genetic - genetics | Research | Gene mutations | Lung cancer | Risk factors
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2010, Volume 120, Issue 1, pp. 142 - 156
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 11, p. e14124
AZD6244 and MK2206 are targeted small-molecule drugs that inhibit MEK and AKT respectively. The efficacy of this combination in lung cancer is unknown. Our... 
PATHWAYS | ACTIVATION | MUTATION STATUS | COLORECTAL-CANCER | KINASE | BIOLOGY | SENSITIVITY | RESISTANCE | KRAS | AZD6244 ARRY-142886 | LINES | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Dose-Response Relationship, Drug | Mitogen-Activated Protein Kinase Kinases - metabolism | Benzimidazoles - administration & dosage | Female | Proto-Oncogene Proteins c-akt - metabolism | Carcinoma, Non-Small-Cell Lung - pathology | Cell Survival - drug effects | Carcinoma, Non-Small-Cell Lung - metabolism | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Drug Synergism | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Tumor Burden - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Mice, Nude | Heterocyclic Compounds, 3-Ring - administration & dosage | Survival Analysis | Cell Line, Tumor | Benzimidazoles - pharmacology | Mice | Mice, Inbred BALB C | Carcinoma, Non-Small-Cell Lung - drug therapy | Cell Cycle - drug effects | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Prevention | Lung cancer, Small cell | Drug therapy, Combination | Lung cancer, Non-small cell | Cancer | Drugs | Therapy | Biotechnology | Laboratories | Heart surgery | Lung cancer | Colorectal cancer | Clinical trials | Oncology | AKT protein | Metastasis | Kinases | Anticancer properties | Proteins | Signal transduction | Cell cycle | Xenografts | Inhibition | Immunoglobulins | Non-small cell lung carcinoma | Extracellular signal-regulated kinase | Tumor cell lines | Survival | Cell lines | Antitumor activity | Mutation | Synergistic effect | BIM protein | Tumors | Apoptosis
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 4044 - 4054
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2006, Volume 103, Issue 24, pp. 9244 - 9249
Mutation in the ABL kinase domain is the principal mechanism of imatinib resistance in patients with chronic myelogenous leukemia. Many mutations favor active... 
Relapse | Mutagenesis | Active sites | Mutagenicity tests | Drug regulation | Point mutation | Disease remission | Drug resistance | Preclinical drug evaluation | Cells | Chronic myelogenous leukemia | Imatinib | Kinase inhibitors | Combination chemotherapy | WILD-TYPE | C-ABL | TYROSINE KINASE | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | combination chemotherapy | BLAST CRISIS | imatinib | chronic myelogenous leukemia | CHRONIC MYELOID-LEUKEMIA | kinase inhibitors | STRUCTURAL BASIS | CLINICAL RESISTANCE | MUTANT BCR-ABL | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Protein-Tyrosine Kinases - metabolism | Pyridines - chemistry | Humans | Piperazines - metabolism | Piperazines - chemistry | Pyrimidines - chemistry | Pyrimidines - metabolism | Protein Kinase Inhibitors - chemistry | Protein-Tyrosine Kinases - genetics | Fusion Proteins, bcr-abl | Adenosine Triphosphate - metabolism | Drug Resistance - physiology | src-Family Kinases - metabolism | Molecular Structure | Protein Structure, Tertiary | Proto-Oncogene Proteins c-abl - genetics | src-Family Kinases - antagonists & inhibitors | Models, Molecular | Imatinib Mesylate | Adenosine Triphosphate - analogs & derivatives | Pyridines - metabolism | Proto-Oncogene Proteins c-abl - metabolism | Benzamides | Mutation | Adenosine Triphosphate - chemistry | src-Family Kinases - genetics | Protein Kinase Inhibitors - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Chemotherapy | Research | Protein kinases | Leukemia | Cancer | Biological Sciences
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2003, Volume 100, Issue 21, pp. 12444 - 12449
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2007, Volume 104, Issue 28, pp. 11832 - 11837
Journal Article
Cell Cycle, ISSN 1538-4101, 12/2006, Volume 5, Issue 23, pp. 2778 - 2786
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, p. e77262
Journal Article
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 7/2008, Volume 100, Issue 13, pp. 926 - 939
Background Imatinib is a tyrosine kinase inhibitor that is used to treat chronic myelogenous leukemia (CML). BCR-ABL mutations are associated with failure of... 
CHRONIC MYELOGENOUS LEUKEMIA | CYTOGENETIC RESPONSES | IN-VITRO | SIGNALING PATHWAYS | ONCOLOGY | TYROSINE KINASE | BLAST CRISIS | CLINICAL RESISTANCE | DOMAIN MUTATIONS | SRC FAMILY KINASES | CHRONIC MYELOID-LEUKEMIA | Phosphorylation | Immunoprecipitation | Apoptosis - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Middle Aged | Immunoblotting | Male | Antineoplastic Agents - therapeutic use | Protein Kinase Inhibitors - adverse effects | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - drug therapy | Caspases - metabolism | Fusion Proteins, bcr-abl | Antineoplastic Agents - adverse effects | Mass Spectrometry | src-Family Kinases - metabolism | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - genetics | Adult | Female | Cell Survival - drug effects | Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative - enzymology | Piperazines - therapeutic use | Enzyme Activation - drug effects | Imatinib Mesylate | Piperazines - adverse effects | Drug Resistance, Neoplasm - genetics | Animals | Mice, Nude | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Pyrimidines - adverse effects | Cell Line, Tumor | Aged | Mice | Benzamides | Protein-Tyrosine Kinases - antagonists & inhibitors | Physiological aspects | Genetic aspects | Chronic myeloid leukemia | Research | Drug therapy | Gene expression | Risk factors | Oncology | Chemotherapy | Cellular biology | Drug resistance | Kinases | Leukemia | Index Medicus
Journal Article