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Journal Article
ISME Journal, ISSN 1751-7362, 2014, Volume 8, Issue 7, pp. 1403 - 1417
Dysregulated immune responses to gut microbes are central to inflammatory bowel disease (IBD), and gut microbial activity can fuel chronic inflammation.... 
treatment | gnotobiotic mice | colitis | gut microbiome | community structure | gut microbiota | LABORATORY MICE | BACTERIA | MESENTERIC LYMPH-NODES | PROBIOTICS | MICROBIOLOGY | IBD | COMMUNITIES | VIRULENCE | DISCOVERY | INFLAMMATORY-BOWEL-DISEASE | ECOLOGY | SP-NOV | Original
Journal Article
Journal of Surgical Research, ISSN 0022-4804, 2015, Volume 193, Issue 2, pp. 745 - 753
Abstract Background Currently, there is no in vitro or ex vivo model that can isolate circulating tumor cells (CTCs). Recently, we developed a four-dimensional... 
Surgery | Ex vivo | 4D model | Circulating tumor cells | Lung cancer | Ex vivo | SURVIVAL | SURGERY | METASTASIS | ANOIKIS | TISSUE | LUNG-CANCER CELLS | GENETIC MOUSE MODEL | Animals | Humans | Cell Line, Tumor | Neoplastic Cells, Circulating - metabolism | Rats | Cell Culture Techniques | In Vitro Techniques | Cell Adhesion | Cell Adhesion Molecules - metabolism | Integrin beta4 - metabolism | Metastasis | Analysis | Integrins
Journal Article
Journal of Medicinal Chemistry, ISSN 0022-2623, 06/2010, Volume 53, Issue 12, pp. 4701 - 4719
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 01/2017, Volume 114, Issue 1, pp. 142 - 147
Journal Article
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 11/2016, Volume 22, Issue 22, pp. 5527 - 5538
Journal Article
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 5, pp. 401 - 412
Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain... 
CHEMBIO | HUMDISEASE | CHRONIC MYELOGENOUS LEUKEMIA | DASATINIB BMS-354825 | MESYLATE | CML | ONCOLOGY | KINASE DOMAIN MUTATIONS | AMN107 | IMATINIB RESISTANCE | NILOTINIB | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Pyridazines - pharmacology | Protein Kinase Inhibitors - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Antineoplastic Agents - pharmacology | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Proto-Oncogene Proteins c-abl - genetics | Cell Growth Processes - drug effects | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-abl - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Chronic myeloid leukemia | BCR protein | Imatinib | Mutagenesis | Abl protein | Mutation | Fusion protein | Tumors | Index Medicus | imatinib resistance | dasatinib | nilotinib | compound mutation
Journal Article
Cancer Chemotherapy and Pharmacology, ISSN 0344-5704, 5/2013, Volume 71, Issue 5, pp. 1315 - 1323
Journal Article
Journal of Medicinal Chemistry, ISSN 0022-2623, 05/2016, Volume 59, Issue 10, pp. 4948 - 4964
In the treatment of echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase positive (ALK+) non-small-cell lung cancer (NSCLC),... 
CELL LUNG-CANCER | WILD-TYPE | CHEMISTRY, MEDICINAL | SRC TYROSINE KINASE | THERAPEUTIC TARGET | RESISTANCE | ATOMS-IN-MOLECULES | ALK INHIBITOR | IDENTIFICATION | ALK/ROS1 INHIBITOR | SMALL-MOLECULE INHIBITOR | Lung Neoplasms - drug therapy | Phosphines - pharmacology | Humans | Molecular Conformation | Lung Neoplasms - pathology | Structure-Activity Relationship | Antineoplastic Agents - administration & dosage | Pyrimidines - chemistry | Dose-Response Relationship, Drug | Neoplasms, Experimental - pathology | Protein Kinase Inhibitors - chemistry | Phosphines - chemistry | Organophosphorus Compounds - pharmacology | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Antineoplastic Agents - pharmacology | Carcinoma, Non-Small-Cell Lung - pathology | Cell Survival - drug effects | Lung Neoplasms - enzymology | Administration, Oral | Pyrimidines - administration & dosage | Rats | Organophosphorus Compounds - chemistry | Pyrimidines - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Receptor Protein-Tyrosine Kinases - metabolism | Drug Discovery | Protein Kinase Inhibitors - administration & dosage | Animals | Receptor Protein-Tyrosine Kinases - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Organophosphorus Compounds - administration & dosage | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Neoplasms, Experimental - drug therapy | Drug Screening Assays, Antitumor
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 11/2014, Volume 20, Issue 22, pp. 5745 - 5755
Purpose: KIT is the major oncogenic driver of gastrointestinal stromal tumors (GIST). Imatinib, sunitinib, and regorafenib are approved therapies; however,... 
EFFICACY | ONCOLOGY | SAFETY | SUNITINIB | C-KIT | MYELOID-LEUKEMIA | MECHANISMS | MUTATIONS | DASATINIB | IMATINIB RESISTANCE | NILOTINIB | Exons | Humans | Molecular Conformation | Imidazoles - chemistry | Tomography, X-Ray Computed | Antineoplastic Agents - therapeutic use | Pyridazines - pharmacology | Proto-Oncogene Proteins c-kit - antagonists & inhibitors | Dose-Response Relationship, Drug | Protein Kinase Inhibitors - chemistry | Gastrointestinal Stromal Tumors - diagnosis | Gastrointestinal Stromal Tumors - pathology | Inhibitory Concentration 50 | Female | Indoles - pharmacology | Proto-Oncogene Proteins c-kit - genetics | Tumor Burden - genetics | Antineoplastic Agents - pharmacology | Benzamides - pharmacology | Imidazoles - therapeutic use | Gastrointestinal Stromal Tumors - genetics | Pyridazines - therapeutic use | Disease Models, Animal | Neoplasm Recurrence, Local | Models, Molecular | Imidazoles - pharmacology | Pyrimidines - pharmacology | Antineoplastic Agents - chemistry | Imatinib Mesylate | Piperazines - pharmacology | Pyridazines - chemistry | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Pyrroles - pharmacology | Animals | Tumor Burden - drug effects | Gastrointestinal Stromal Tumors - drug therapy | Protein Kinase Inhibitors - therapeutic use | Cell Line, Tumor | Protein Binding | Protein Kinase Inhibitors - pharmacology | Mutation | Proto-Oncogene Proteins c-kit - chemistry | Index Medicus | GIST | ponatinib | tyrosine kinase inhibitor | resistance | KIT
Journal Article
Journal Article
Cancer Research, ISSN 0008-5472, 08/2015, Volume 75, Issue 15 Supplement, pp. 781 - 781
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 06/2011, Volume 10, Issue 6, pp. 1028 - 1035
Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels. Ponatinib... 
MUTANT | ACTIVATION | ONCOLOGY | FLT3 | RESISTANCE | TYROSINE KINASES | MUTATIONS