Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back.
about
Two different point mutations in ABL gene ATP-binding domain conferring primary imatinib resistance in a chronic myeloid leukemia (CML) patient: A case reportGrowth arrest of BCR-ABL positive cells with a sequence-specific polyamide-chlorambucil conjugateDynamics of resistance development to imatinib under increasing selection pressure: a combination of mathematical models and in vitro dataIdentification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemiasDissection of PIM serine/threonine kinases in FLT3-ITD-induced leukemogenesis reveals PIM1 as regulator of CXCL12-CXCR4-mediated homing and migration.Oncogenic stress induced by acute hyper-activation of Bcr-Abl leads to cell death upon induction of excessive aerobic glycolysis.A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.Overcoming CML acquired resistance by specific inhibition of Aurora A kinase in the KCL-22 cell model.Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance.PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.Advances and potential treatment for Philadelphia chromosome-positive adult acute lymphoid leukaemia.Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia.Chronic Myeloid Leukaemia in The 21st Century.Inhibition of Hsp90 activates osteoclast c-Src signaling and promotes growth of prostate carcinoma cells in boneImatinib mesylate in the treatment of hematologic malignancies.Treatment of Philadelphia chromosome-positive adult acute lymphoblastic leukemia.Managing Philadelphia chromosome-positive acute lymphoblastic leukemia: role of tyrosine kinase inhibitors.Philadelphia chromosome-positive leukemia stem cells in acute lymphoblastic leukemia and tyrosine kinase inhibitor therapy.Management options for refractory chronic myeloid leukemia: considerations for the elderly.Forced expression of Wnt antagonists sFRP1 and WIF1 sensitizes chronic myeloid leukemia cells to tyrosine kinase inhibitors.Cobll1 is linked to drug resistance and blastic transformation in chronic myeloid leukemia.Mechanisms of Resistance to ABL Kinase Inhibition in Chronic Myeloid Leukemia and the Development of Next Generation ABL Kinase Inhibitors.An investigation of reversal of imatinib resistance in the Bcr-Abl positive imatinib-resistant cell line K562r by dasatinib, nilotinib, rapamycin and bortezomib.Inhibition of Abl tyrosine kinase enhances nerve growth factor-mediated signaling in Bcr-Abl transformed cells via the alteration of signaling complex and the receptor turnover.Synergistic interactions between MEK1/2 and histone deacetylase inhibitors in BCR/ABL+ human leukemia cells.Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity.Global effects of BCR/ABL and TEL/PDGFRbeta expression on the proteome and phosphoproteome: identification of the Rho pathway as a target of BCR/ABL.Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate.Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells.Phosphorylation of tyrosine 393 in the kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo.Contributions of MET activation to BCR-ABL1 tyrosine kinase inhibitor resistance in chronic myeloid leukemia cells.Self-inactivating lentiviral vectors resist proviral methylation but do not confer position-independent expression in hematopoietic stem cells.In vitro drug resistance to imatinib and mutation of ABL gene in childhood Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia.Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant.Prevalence and dynamics of bcr-abl kinase domain mutations during imatinib treatment differ in patients with newly diagnosed and recurrent bcr-abl positive acute lymphoblastic leukemia.BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?
P2860
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P2860
Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back.
description
2003 nî lūn-bûn
@nan
2003 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@ast
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@en
type
label
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@ast
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@en
prefLabel
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@ast
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@en
P2093
P2860
P356
P1433
P1476
Resistance of Philadelphia-chr ...... eted oncoprotein strikes back.
@en
P2093
von Bubnoff N
P2860
P2888
P304
P356
10.1038/SJ.LEU.2402889
P577
2003-05-01T00:00:00Z