High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.
about
Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndromeA screen to identify drug resistant variants to target-directed anti-cancer agentsWhat a tangled web we weave: emerging resistance mechanisms to inhibition of the phosphoinositide 3-kinase pathwayScreening approaches to generating STAT inhibitors: Allowing the hits to identify the targetsCurrent concepts in pediatric Philadelphia chromosome-positive acute lymphoblastic leukemiaTargeting Bcr–Abl by combining allosteric with ATP-binding-site inhibitorsAxitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformationDissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.Random mutagenesis reveals residues of JAK2 critical in evading inhibition by a tyrosine kinase inhibitorInhibition of Aurora kinase B is important for biologic activity of the dual inhibitors of BCR-ABL and Aurora kinases R763/AS703569 and PHA-739358 in BCR-ABL transformed cellsBCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Conformational disturbance in Abl kinase upon mutation and deregulation.BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability.Eradication of chronic myeloid leukemia stem cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinibApplication of a haematopoetic progenitor cell-targeted adeno-associated viral (AAV) vector established by selection of an AAV random peptide library on a leukaemia cell line.New approved dasatinib regimen available for clinical use.Subcutaneous omacetaxine mepesuccinate in patients with chronic-phase chronic myeloid leukemia previously treated with 2 or more tyrosine kinase inhibitors including imatinib.The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data.K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate.In-vitro and in-vivo combined effect of ARQ 092, an AKT inhibitor, with ARQ 087, a FGFR inhibitor.Resistance to 1,25D-induced differentiation in human acute myeloid leukemia HL60-40AF cells is associated with reduced transcriptional activity and nuclear localization of the vitamin D receptor.Efficacy of escalated imatinib combined with cytarabine in newly diagnosed patients with chronic myeloid leukemiaOncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutationInhibition of calcineurin combined with dasatinib has direct and indirect anti-leukemia effects against BCR-ABL1(+) leukemia.A structure-guided approach to creating covalent FGFR inhibitorsOverlooking evolution: a systematic analysis of cancer relapse and therapeutic resistance research.Targeting abnormal DNA double-strand break repair in tyrosine kinase inhibitor-resistant chronic myeloid leukemias.Chronic myelogenous leukemia: treatment and monitoring.The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors.Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML.Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Is there a cloud in the silver lining for imatinib?Perspectives on the treatment of chronic phase and advanced phase CML and Philadelphia chromosome positive ALL(1).Clinical applications of BCR-ABL molecular testing in acute leukemiaResistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back.A method for screening and validation of resistant mutations against kinase inhibitorsBCR-ABL suppresses autophagy through ATF5-mediated regulation of mTOR transcriptionStem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitorsMultiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors.
P2860
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P2860
High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh-hant
name
High frequency of point mutati ...... imatinib (STI571) resistance.
@en
High frequency of point mutati ...... leukemia who develop imatinib
@nl
type
label
High frequency of point mutati ...... imatinib (STI571) resistance.
@en
High frequency of point mutati ...... leukemia who develop imatinib
@nl
prefLabel
High frequency of point mutati ...... imatinib (STI571) resistance.
@en
High frequency of point mutati ...... leukemia who develop imatinib
@nl
P2093
P921
P356
P1433
P1476
High frequency of point mutati ...... imatinib (STI571) resistance.
@en
P2093
Andrew Grigg
Chris Arthur
Kerry Taylor
Kevin P Lynch
Richard Herrmann
Sonya Walsh
Susan Branford
Timothy P Hughes
Zbigniew Rudzki
P304
P356
10.1182/BLOOD.V99.9.3472
P407
P577
2002-05-01T00:00:00Z