BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism. - Wikidata - wikimedia - TriplyDB

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

http://www.wikidata.org/entity/Q40021043

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Mechanisms of drug resistance in kinases.IL-3 and oncogenic Abl regulate the myeloblast transcriptome by altering mRNA stability.A chemical biology approach to developing STAT inhibitors: molecular strategies for accelerating clinical translation Exploiting mitochondrial dysfunction for effective elimination of imatinib-resistant leukemic cells.In acute myeloid leukemia, B7-H1 (PD-L1) protection of blasts from cytotoxic T cells is induced by TLR ligands and interferon-gamma and can be reversed using MEK inhibitors.Small sizes and indolent evolutionary dynamics challenge the potential role of P2RY8-CRLF2-harboring clones as main relapse-driving force in childhood ALL.The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors.GILZ inhibits the mTORC2/AKT pathway in BCR-ABL(+) cells.The STAT5 Inhibitor Pimozide Displays Efficacy in Models of Acute Myelogenous Leukemia Driven by FLT3 Mutations Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia.Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.Blocking cytokine signaling along with intense Bcr-Abl kinase inhibition induces apoptosis in primary CML progenitors.Clinical impact of low-burden BCR-ABL1 mutations detectable by amplicon deep sequencing in Philadelphia-positive acute lymphoblastic leukemia patients.Omacetaxine mepesuccinate prevents cytokine-dependent resistance to nilotinib in vitro: potential role of the common β-subunit c of cytokine receptors.

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P2860

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

http://www.wikidata.org/entity/Q40021043

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

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type

label

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

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prefLabel

BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

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BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.

@en

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B Quesnel

http://www.w3.org/2001/XMLSchema#string

C Preudhomme

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D Hetuin

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J Liu

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N Philippe

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S Corm

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S Joha

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T Idziorek

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P2860

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

The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.

Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.

Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis

Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance.

Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.

Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.

MEK1/2 inhibitors sensitize Bcr/Abl+ human leukemia cells to the dual Abl/Src inhibitor BMS-354/825

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791-799

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scholarly article

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10.1038/LEU.2008.3

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4

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22

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5634583

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1031739033

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