The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile - Wikidata - wikimedia - TriplyDB

The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile

The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile

http://www.wikidata.org/entity/Q35506849

about

Nilotinib and MEK inhibitors induce synthetic lethality through paradoxical activation of RAF in drug-resistant chronic myeloid leukemia Role of tyrosine-kinase inhibitors in myeloproliferative neoplasms: comparative lessons learned Management of Chronic Myeloid Leukemia Patients Resistant to Tyrosine Kinase Inhibitors Treatment The growing arsenal of ATP-competitive and allosteric inhibitors of BCR-ABL Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD Resistant 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-PDGFRα Drug resistance missense mutations in cancer are subject to evolutionary constraints Abl kinase constructs expressed in bacteria: facilitation of structural and functional studies including segmental labeling by expressed protein ligation Dual 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 relationships The Role of New Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia Ponatinib 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 weapons Anti-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 FoxM1 Rapid 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.

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The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile

http://www.wikidata.org/entity/Q35506849

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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The ABL switch control inhibit ...... ts a narrow resistance profile

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The ABL switch control inhibit ...... ts a narrow resistance profile

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0008-5472.CAN-10-3224

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Cancer Research

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The ABL switch control inhibit ...... ts a narrow resistance profile

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Bryan D Smith

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Christopher A Eide

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Daniel L Flynn

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David J Anderson

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Lauren T Adrian

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Mary Mac Partlin

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Michael W N Deininger

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Peter A Petillo

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Scott C Wise

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Thomas O'Hare

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P2860

AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance

Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency

Targeting Bcr–Abl by combining allosteric with ATP-binding-site inhibitors

Discovery of a small-molecule type II inhibitor of wild-type and gatekeeper mutants of BCR-ABL, PDGFR , Kit, and Src kinases: novel type II inhibitor of gatekeeper mutants

Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance.

Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.

Targeted CML therapy: controlling drug resistance, seeking cure.

SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib.

Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.

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3189-3195

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10.1158/0008-5472.CAN-10-3224

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9

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71

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Brian J. Druker

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2011-04-19T00:00:00Z

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21505103

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chronic myeloid leukemia

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3206627

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