Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
about
Delineation of Polypharmacology across the Human Structural Kinome Using a Functional Site Interaction Fingerprint ApproachOncogenic kinase fusions: an evolving arena with innovative clinical opportunitiesPrecision medicine for cancer with next-generation functional diagnosticsPolypharmacology in Precision Oncology: Current Applications and Future ProspectsBosutinib as a fourth-line therapy for a patient with T315I-positive lymphoid blastic phase chronic myeloid leukemia: A case report.Novel drug candidates for blast phase chronic myeloid leukemia from high-throughput drug sensitivity and resistance testing.Discovery of Novel Antiangiogenic Marine Natural Product Scaffolds.The Emerging Role of ABL Kinases in Solid Tumors.Pharmacological targeting of VEGFR signaling with axitinib inhibits Tsc2-null lesion growth in the mouse model of lymphangioleiomyomatosisBest Practices in Chronic Myeloid Leukemia Monitoring and ManagementA Receptor Tyrosine Kinase Inhibitor, Dovitinib (TKI-258), Enhances BMP-2-Induced Osteoblast Differentiation In Vitro.Extreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive leukemia.Axitinib blocks Wnt/β-catenin signaling and directs asymmetric cell division in cancerExploiting Temporal Collateral Sensitivity in Tumor Clonal Evolution.The spatial organization of intra-tumour heterogeneity and evolutionary trajectories of metastases in hepatocellular carcinoma.Individualized network-based drug repositioning infrastructure for precision oncology in the panomics era.Identification of drug candidates and repurposing opportunities through compound-target interaction networks.Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cellsInformatics Approaches for Predicting, Understanding, and Testing Cancer Drug Combinations.Computational analysis of ABL kinase mutations allows predicting drug sensitivity against selective kinase inhibitors.The development of agents targeting the BCR-ABL tyrosine kinase as Philadelphia chromosome-positive acute lymphoblastic leukemia treatment.From drug response profiling to target addiction scoring in cancer cell models.How has treatment changed for blast phase chronic myeloid leukemia patients in the tyrosine kinase inhibitor era? A review of efficacy and safety.Integrating functional genomics to accelerate mechanistic personalized medicine.Emerging Role of Tyrosine Kinases as Drugable Targets in Cancer.Ex vivo drug response profiling detects recurrent sensitivity patterns in drug-resistant acute lymphoblastic leukemia.Therapeutic targeting of the angiopoietin-TIE pathway.Mechanisms of Resistance to ABL Kinase Inhibition in Chronic Myeloid Leukemia and the Development of Next Generation ABL Kinase Inhibitors.Metabolic characterization of imatinib-resistant BCR-ABL T315I chronic myeloid leukemia cells indicates down-regulation of glycolytic pathway and low ROS production.Discovery of novel drug sensitivities in T-PLL by high-throughput ex vivo drug testing and mutation profiling.Precision Cancer Medicine in the Acoustic Dispensing Era: Ex Vivo Primary Cell Drug Sensitivity Testing.MediSyn: uncertainty-aware visualization of multiple biomedical datasets to support drug treatment selectionCharacteristics and mutation analysis of Ph-positive leukemia patients with T315I mutation receiving tyrosine kinase inhibitors.Network modeling of kinase inhibitor polypharmacology reveals pathways targeted in chemical screens.Anti-leukemic activity of axitinib against cells harboring the BCR-ABL T315I point mutationNovel TKI-resistant BCR-ABL1 gatekeeper residue mutations retain in vitro sensitivity to axitinib.Drug Target Commons: A Community Effort to Build a Consensus Knowledge Base for Drug-Target Interactions.Improving the efficacy-safety balance of polypharmacology in multi-target drug discovery.Drug-perturbation-based stratification of blood cancer.Methods for High-throughput Drug Combination Screening and Synergy Scoring.
P2860
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P2860
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
description
2015 nî lūn-bûn
@nan
2015 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2015 թվականի մարտին հրատարակված գիտական հոդված
@hy
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
name
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@ast
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@en
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@nl
type
label
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@ast
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@en
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@nl
prefLabel
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@ast
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@en
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@nl
P2093
P2860
P50
P3181
P356
P1433
P1476
Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation
@en
P2093
Brion W Murray
Ciarán N Cronin
Eric Johnson
Jeffrey Chen
Michele McTigue
Mika Kontro
Peter Wells
P2860
P2888
P304
P3181
P356
10.1038/NATURE14119
P407
P577
2015-03-05T00:00:00Z
P5875
P6179
1004586276