The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile
about
Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemiaRole of tyrosine-kinase inhibitors in myeloproliferative neoplasms: comparative lessons learnedManagement of Chronic Myeloid Leukemia Patients Resistant to Tyrosine Kinase Inhibitors TreatmentThe growing arsenal of ATP-competitive and allosteric inhibitors of BCR-ABLActivity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITDResistant mutations in CML and Ph(+)ALL - role of ponatinib.The conformational control inhibitor of tyrosine kinases DCC-2036 is effective for imatinib-resistant cells expressing T674I FIP1L1-PDGFRαDrug resistance missense mutations in cancer are subject to evolutionary constraintsAbl kinase constructs expressed in bacteria: facilitation of structural and functional studies including segmental labeling by expressed protein ligationDual function of TGFβ in lens epithelial cell fate: implications for secondary cataract.BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability.Identification of potent Yes1 kinase inhibitors using a library screening approach.Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia.The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Managing chronic myeloid leukemia patients intolerant to tyrosine kinase inhibitor therapy.Targeting the KIT activating switch control pocket: a novel mechanism to inhibit neoplastic mast cell proliferation and mast cell activation.BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationshipsThe Role of New Tyrosine Kinase Inhibitors in Chronic Myeloid LeukemiaPonatinib efficiently kills imatinib-resistant chronic eosinophilic leukemia cells harboring gatekeeper mutant T674I FIP1L1-PDGFRα: roles of Mcl-1 and β-catenin.Genetic mechanisms of chronic myeloid leukemia blastic transformation.Advances in treatment of chronic myeloid leukemia with tyrosine kinase inhibitors: the evolving role of Bcr-Abl mutations and mutational analysis.Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia.Gastrointestinal stromal tumors: what do we know now?Combination therapy with nilotinib for drug-sensitive and drug-resistant BCR-ABL-positive leukemia and other malignancies.Bcr-Abl tyrosine kinase inhibitors: a patent review.Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML.Development of 'DFG-out' inhibitors of gatekeeper mutant kinases.BCR-ABL1 kinase: hunting an elusive target with new weaponsAnti-oxidant vitamin E prevents accumulation of imatinib-resistant BCR-ABL1 kinase mutations in CML-CP xenografts in NSG mice.Genetic progression in gastrointestinal stromal tumors: mechanisms and molecular interventions.CT-721, a Potent Bcr-Abl Inhibitor, Exhibits Excellent In Vitro and In Vivo Efficacy in the Treatment of Chronic Myeloid Leukemia.Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.Improved coiled-coil design enhances interaction with Bcr-Abl and induces apoptosis.BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1Rapid recognition of drug-resistance/sensitivity in leukemic cells by Fourier transform infrared microspectroscopy and unsupervised hierarchical cluster analysis.Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy.
P2860
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P2860
The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile
description
2011 nî lūn-bûn
@nan
2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
The ABL switch control inhibit ...... ts a narrow resistance profile
@ast
The ABL switch control inhibit ...... ts a narrow resistance profile
@en
type
label
The ABL switch control inhibit ...... ts a narrow resistance profile
@ast
The ABL switch control inhibit ...... ts a narrow resistance profile
@en
prefLabel
The ABL switch control inhibit ...... ts a narrow resistance profile
@ast
The ABL switch control inhibit ...... ts a narrow resistance profile
@en
P2093
P2860
P1433
P1476
The ABL switch control inhibit ...... ts a narrow resistance profile
@en
P2093
Bryan D Smith
Christopher A Eide
Daniel L Flynn
David J Anderson
Lauren T Adrian
Mary Mac Partlin
Michael W N Deininger
Peter A Petillo
Scott C Wise
Thomas O'Hare
P2860
P304
P356
10.1158/0008-5472.CAN-10-3224
P407
P577
2011-04-19T00:00:00Z