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Nature Medicine, ISSN 1078-8956, 04/2012, Volume 18, Issue 4, pp. 521 - 528
Tyrosine kinase inhibitors (TKIs) elicit high response rates among individuals with kinase-driven malignancies, including chronic myeloid leukemia (CML) and... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | GEFITINIB | BIOCHEMISTRY & MOLECULAR BIOLOGY | EYE DISEASES | CHRONIC MYELOID-LEUKEMIA | CELL BIOLOGY | CELL LUNG-CANCER | FACTOR RECEPTOR EGFR | GROWTH | ACTIVATING MUTATIONS | MUTANT EGFR | Enzyme-Linked Immunosorbent Assay - methods | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Follow-Up Studies | Apoptosis - drug effects | Humans | Middle Aged | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Male | BH3 Interacting Domain Death Agonist Protein - genetics | Dose-Response Relationship, Drug | Protein Isoforms - metabolism | Transfection | Bcl-2-Like Protein 11 | Statistics, Nonparametric | Aged, 80 and over | Apoptosis Regulatory Proteins - genetics | Adult | Female | Gene Expression Regulation, Neoplastic - drug effects | Lung Neoplasms - genetics | Annexins - metabolism | Carcinoma, Non-Small-Cell Lung - genetics | Membrane Proteins - genetics | Gene Frequency | Exons - genetics | Genotype | Proto-Oncogene Proteins - genetics | International Cooperation | Drug Resistance, Neoplasm - genetics | Cell Line, Tumor | Polymorphism, Genetic - genetics | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Cohort Studies | Drug Resistance, Neoplasm - drug effects | Protein Isoforms - genetics | RNA, Small Interfering - metabolism | Sequence Deletion - genetics | Antimitotic agents | Physiological aspects | Protein tyrosine kinase | Dosage and administration | Genetic aspects | Research | Antineoplastic agents | Tumor proteins | Genetic polymorphisms | Inhibitor drugs | Mutation | Kinases | Gene expression | Apoptosis | Polymorphism | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 06/2013, Volume 110, Issue 25, pp. E2298 - E2307
Chronic myeloid leukemia responds well to therapy targeting the oncogenic fusion protein BCR-ABL1 in chronic phase, but is resistant to treatment after it... 
Cancer stem cell | Biomarker | Xenograft | Wnt pathway | CHRONIC MYELOGENOUS LEUKEMIA | MOLECULAR-BIOLOGY | MULTIDISCIPLINARY SCIENCES | BCR-ABL | KINASE 1 | TRANSLATION INITIATION | biomarker | BETA-CATENIN | PROTEIN-SYNTHESIS | cancer stem cell | xenograft | MESSENGER-RNA | EIF4E PHOSPHORYLATION | SIGNALING PATHWAY | Phosphorylation - physiology | RNA, Small Interfering - genetics | Blast Crisis - drug therapy | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Eukaryotic Initiation Factor-4E - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Neoplastic Stem Cells - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Neoplastic Stem Cells - pathology | Female | Protein-Serine-Threonine Kinases - metabolism | Aniline Compounds - pharmacology | Blast Crisis - pathology | Purines - pharmacology | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Bone Marrow Cells - pathology | beta Catenin - metabolism | Xenograft Model Antitumor Assays | Animals | K562 Cells | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice, Inbred NOD | Mice | Protein Kinase Inhibitors - pharmacology | Blast Crisis - metabolism | Bone Marrow Cells - metabolism | Signal transduction | Phosphorylation | Leukemia | Stem cells | Pharmacology | Kinases | Gene expression | Index Medicus | Biological Sciences | PNAS Plus
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2017, Volume 12, Issue 3, pp. e0174107 - e0174107
Chronic myeloid leukemia (CML) treatment has been improved by tyrosine kinase inhibitors (TKIs) such as imatinib mesylate (IM) but various factors can cause... 
CELLS | DOMAIN | CML | THERAPY | ACETYLATION | MULTIDISCIPLINARY SCIENCES | IMATINIB | HISTONE DEACETYLASE INHIBITORS | COMBINATION | CANCER | CHAPERONE FUNCTION | Apoptosis - drug effects | Humans | Enzyme Inhibitors - pharmacology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Bcl-2-Like Protein 11 - genetics | RNA Splicing | Gene Deletion | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Fusion Proteins, bcr-abl - antagonists & inhibitors | K562 Cells | Benzimidazoles - pharmacology | Histone Deacetylase Inhibitors - pharmacology | Antineoplastic Agents - pharmacology | Care and treatment | Analysis | Genetic aspects | Chronic myeloid leukemia | Research | Risk factors | Genetic polymorphisms | Cancer | BCR protein | Biotechnology | Histone deacetylase | Chromatin | Substance abuse treatment | Leukemia | Lung cancer | Biology | mRNA | Gene deletion | Kinases | Gene polymorphism | Cancer therapies | Medical schools | Proteins | Clonal deletion | Rodents | Deletion | Fusion protein | Growth factors | Protein-tyrosine kinase | Tyrosine | Medical research | Imatinib | Immunoglobulins | Hematology | Splicing | Review boards | Myeloid leukemia | Hydroxamic acid | Abl protein | Pharmacology | Gene expression | Patients | Resistance factors | Hospitals | Inhibitors | Cell death | Cell lines | Isoforms | Stem cells | Viability | BIM protein | Apoptosis | Polymorphism | Index Medicus
Journal Article
Journal Article
Oncotarget, ISSN 1949-2553, 2014, Volume 5, Issue 19, pp. 9033 - 9038
BCR-ABL1-specific tyrosine kinase inhibitors prolong the life of patients with chronic myeloid leukemia (CML) but cannot completely eradicate CML progenitors.... 
Imatinib | CML | Progenitors | Normal cord blood | ABT-199 | BH3 mimetic | Index Medicus
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2013, Volume 110, Issue 25, pp. 10061 - 10061
Journal Article
by Thorsson, Vesteinn and Thorsson, Vésteinn and Gibbs, Richard A and Gibbs, David L and Brown, Scott D and Wolf, Gregory and Wolf, Denise and Bortone, Dante S and Ou Yang, Tai-Hsien and Porta-Pardo, Eduard and Gao, Galen F and Gao, Jianjiong and Plaisier, Christopher L and Eddy, James A and Ziv, Elad and Culhane, Aedin C and Paull, Evan O and Sivakumar, I.K. Ashok and Gentles, Andrew J and Malhotra, Raunaq and Farshidfar, Farshad and Colaprico, Antonio and Parker, Joel S and Mose, Lisle E and Vo, Nam Sy and Liu, Wenbin and Liu, Jianfang and Liu, Jia and Liu, Yuexin and Liu, Xiuping and Rader, Janet and Dhankani, Varsha and Reynolds, Sheila and Reynolds, Sheila M and Bowlby, Reanne and Califano, Andrea and Cherniack, Andrew D and Anastassiou, Dimitris and Bedognetti, Davide and Mokrab, Younes and Newman, Aaron M and Rao, Arvind and Chen, Amy and Chen, Chu and Chen, Ken and Krasnitz, Alexander and Hu, Jianhong and Hu, Hai and Malta, Tathiane M and Noushmehr, Houtan and Pedamallu, Chandra Sekhar and Bullman, Susan and Ojesina, Akinyemi I and Lamb, Andrew and Zhou, Wanding and Shen, Hui and Choueiri, Toni K and Weinstein, John N and Guinney, Justin and Saltz, Joel and Holt, Robert and Holt, Robert A and Rabkin, Charles S and Caesar-Johnson, Samantha J and Demchok, John A and Felau, Ina and Kasapi, Melpomeni and Ferguson, Martin L and Hutter, Carolyn M and Sofia, Heidi J and Tarnuzzer, Roy and Wang, Jioajiao and Wang, Min and Wang, Linghua and Wang, Zhining and Wang, Timothy and Wang, Jing and Yang, Ju Dong and Yang, Hannah and Yang, Liming and Yang, Ian and Zenklusen, Jean C and Zhang, Jiashan (Julia) and Zhang, Jiexin and Zhang, Lizhi and Zhang, Wei and Zhang, Hongzheng and Zhang, Hailei and Zhang, Hongxin and Chudamani, Sudha and Lolla, Laxmi and Naresh, Rashi and Pihl, Todd and Sun, Yichao and Sun, Qiang and Wan, Yunhu and Wu, Ye and Cho, Juok and DeFreitas, Timothy and Frazer, Scott and ... and Canc Genome Atlas Res Network and Cancer Genome Atlas Research Network
Immunity, ISSN 1074-7613, 04/2018, Volume 48, Issue 4, pp. 812 - 830.e14
We performed an extensive immunogenomic analysis of more than 10,000 tumors comprising 33 diverse cancer types by utilizing data compiled by TCGA. Across... 
tumor immunology | immunotherapy | cancer genomics | integrative network analysis | immuno-oncology | tumor microenvironment | immune subtypes | immunomodulatory | GENOMIC ANALYSES | INFORMATION | T-CELL-RECEPTOR | REGULATORY NETWORK | CLASSIFICATION | IMMUNOLOGY | SEQUENCING DATA | SOMATIC MUTATIONS | COMPREHENSIVE ANALYSIS | PREDICTION | REVEALS | Transforming Growth Factor beta - immunology | Prognosis | Humans | Middle Aged | Th1-Th2 Balance - physiology | Male | Neoplasms - classification | Wound Healing - immunology | Young Adult | Transforming Growth Factor beta - genetics | Neoplasms - genetics | Neoplasms - immunology | Interferon-gamma - immunology | Adolescent | Aged, 80 and over | Adult | Female | Aged | Interferon-gamma - genetics | Wound Healing - genetics | Genomics - methods | Child | Macrophages - immunology | Cell proliferation | Cluster analysis | Transcription | Copy number | p53 Protein | Lung cancer | Genomics | Aneuploidy | Lymphocytes T | Genomes | Cell interactions | Macrophages | Immunotherapy | DNA methylation | Deoxyribonucleic acid--DNA | Immune system | Medical research | Wound healing | Immunomodulation | MiRNA | Stockholders | Inflammation | T cell receptors | Communications networks | Gene expression | White blood cells | Inventors | Medical prognosis | γ-Interferon | Mutation | Cancer | Tumors | Index Medicus | Immune Subtypes | Integrative Network Analysis | Cancer Genomics | Immuno-oncology | Tumor immunology
Journal Article