Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.
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Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cellsIdentification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemiasPhotocleavable peptide-conjugated magnetic beads for protein kinase assays by MALDI-TOF MSSpred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cellsPhase I and pharmacological study of cytarabine and tanespimycin in relapsed and refractory acute leukemia.The bone marrow microenvironment as a sanctuary for minimal residual disease in CML.Hsp90 inhibitors and drug resistance in cancer: the potential benefits of combination therapies of Hsp90 inhibitors and other anti-cancer drugsInhibition of heat shock protein 90 prolongs survival of mice with BCR-ABL-T315I-induced leukemia and suppresses leukemic stem cells.Selective and cell-active inhibitors of the USP1/ UAF1 deubiquitinase complex reverse cisplatin resistance in non-small cell lung cancer cellsDrug-drug interactions between moxifloxacin and rifampicin based on pharmacokinetics in vivo in rats.PI3K-independent mTOR activation promotes lapatinib resistance and IAP expression that can be effectively reversed by mTOR and Hsp90 inhibitionc-Abl Mediated Tyrosine Phosphorylation of Aha1 Activates Its Co-chaperone Function in Cancer Cells.Heat Shock Protein 90 is overexpressed in high-risk myelodysplastic syndromes and associated with higher expression and activation of Focal Adhesion KinaseP-Glycoprotein-mediated resistance to Hsp90-directed therapy is eclipsed by the heat shock response.The novel HSP90 inhibitor STA-9090 exhibits activity against Kit-dependent and -independent malignant mast cell tumorsHeat shock protein 90 inhibitors: new mode of therapy to overcome endocrine resistance.Synergistic effects of proteasome inhibitor carfilzomib in combination with tyrosine kinase inhibitors in imatinib-sensitive and -resistant chronic myeloid leukemia models.Overcoming resistance in chronic myelogenous leukemia.Glucocorticoid Receptor-Targeted Liposomal Codelivery of Lipophilic Drug and Anti-Hsp90 Gene: Strategy to Induce Drug-Sensitivity, EMT-Reversal, and Reduced Malignancy in Aggressive Tumors.Novel therapeutic strategies in multiple myeloma: role of the heat shock protein inhibitors.Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.HSP90 inhibition results in apoptosis of Philadelphia acute lymphoblastic leukaemia cells: an attractive prospect of new targeted agents.The synthetic heat shock protein 90 (Hsp90) inhibitor EC141 induces degradation of Bcr-Abl p190 protein and apoptosis of Ph-positive acute lymphoblastic leukemia cells.Plerixafor inhibits chemotaxis toward SDF-1 and CXCR4-mediated stroma contact in a dose-dependent manner resulting in increased susceptibility of BCR-ABL+ cell to Imatinib and Nilotinib.Inhibition of apoptosis by downregulation of hBex1, a novel mechanism, contributes to the chemoresistance of Bcr/Abl+ leukemic cells.Regulation of survivin expression through Bcr-Abl/MAPK cascade: targeting survivin overcomes imatinib resistance and increases imatinib sensitivity in imatinib-responsive CML cells.Significance of heat-shock protein (HSP) 90 expression in acute myeloid leukemia cells.Targeting Hsp90 by 17-AAG in leukemia cells: mechanisms for synergistic and antagonistic drug combinations with arsenic trioxide and Ara-C.Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia.Membrane perturbation through novel cell-penetrating peptides influences intracellular accumulation of imatinib mesylate in CML cells.In vitro testing of drug combinations employing nilotinib and alkylating agents with regard to pretransplant conditioning treatment of advanced-phase chronic myeloid leukemia.Cryptotanshinone acts synergistically with imatinib to induce apoptosis of human chronic myeloid leukemia cells.
P2860
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P2860
Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh-hant
name
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@en
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@nl
type
label
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@en
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@nl
prefLabel
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@en
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@nl
P2093
P2860
P356
P1433
P1476
Synergistic activity of imatin ...... ycoprotein function by 17-AAG.
@en
P2093
Fruehauf S
Radujkovic A
Schultheis BS
Veldwijk MR
P2860
P2888
P304
P356
10.1038/SJ.LEU.2403764
P577
2005-07-01T00:00:00Z