All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib. - Wikidata - awgldk - TriplyDB

All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.

All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.

http://www.wikidata.org/entity/Q36926106

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Molecular Determinants Underlying Binding Specificities of the ABL Kinase Inhibitors: Combining Alanine Scanning of Binding Hot Spots with Network Analysis of Residue Interactions and Coevolution A Cell-Based Assay for Measuring Endogenous BcrAbl Kinase Activity and Inhibitor Resistance Latest progress in tyrosine kinase inhibitors Genomic quantitative real-time PCR proves residual disease positivity in more than 30% samples with negative mRNA-based qRT-PCR in Chronic Myeloid Leukemia Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRα-expressing cells Real-time analysis of imatinib- and dasatinib-induced effects on chronic myelogenous leukemia cell interaction with fibronectin.BIRC6 mediates imatinib resistance independently of Mcl-1.Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment Induction of apoptosis by directing oncogenic Bcr-Abl into the nucleus.Therapy of chronic myeloid leukemia: twilight of the imatinib era?The novel anticancer agent JNJ-26854165 is active in chronic myeloid leukemic cells with unmutated BCR/ABL and T315I mutant BCR/ABL through promoting proteosomal degradation of BCR/ABL proteins.Depression of oncogenecity by dephosphorylating and degrading BCR-ABL.Current perspectives on the therapeutic aspects of chronic myelogenous leukemia.Do we need more drugs for chronic myeloid leukemia?A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib.Ponatinib in the therapy of chronic myeloid leukemia.Combined effects of PI3K and SRC kinase inhibitors with imatinib on intracellular calcium levels, autophagy, and apoptosis in CML-PBL cells.Modeling the influence of stromal microenvironment in the selection of ENU-induced BCR-ABL1 mutants by tyrosine kinase inhibitors.Targeting BCR-ABL-Independent TKI Resistance in Chronic Myeloid Leukemia by mTOR and Autophagy Inhibition.Targeting the Extracellular Signal-Regulated Kinase 5 Pathway to Suppress Human Chronic Myeloid Leukemia Stem Cells

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All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.

http://www.wikidata.org/entity/Q36926106

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

All tyrosine kinase inhibitor- ...... highly sensitive to ponatinib.

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type

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All tyrosine kinase inhibitor- ...... highly sensitive to ponatinib.

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All tyrosine kinase inhibitor- ...... highly sensitive to ponatinib.

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All tyrosine kinase inhibitor- ...... highly sensitive to ponatinib.

@en

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Alexandre Puissant

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

Alix Dubois

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

Amine Hamouda

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

Arnaud Jacquel

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

Clémence Ginet

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

Fredéric Luciano

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

Guillaume Robert

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

Jean-Michel Karsenti

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

Jill Patrice Cassuto

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

Laurence Legros

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

P2860

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

Structural mechanism of the Pan-BCR-ABL inhibitor ponatinib (AP24534): lessons for overcoming kinase inhibitor resistance

Acadesine kills chronic myelogenous leukemia (CML) cells through PKC-dependent induction of autophagic cell death

The non-receptor tyrosine kinase Lyn controls neutrophil adhesion by recruiting the CrkL-C3G complex and activating Rap1 at the leading edge

Discovery of 3-[2-(imidazo[1,2-b]pyridazin-3-yl)ethynyl]-4-methyl-N-{4-[(4-methylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl}benzamide (AP24534), a potent, orally active pan-inhibitor of breakpoint cluster region-abelson (BCR-ABL) kinase includ

The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia.

Chronic myeloid leukemia stem cells in the era of targeted therapies: resistance, persistence and long-term dormancy.

Mechanisms of AXL overexpression and function in Imatinib-resistant chronic myeloid leukemia cells.

BCL2L10 is a predictive factor for resistance to azacitidine in MDS and AML patients.

Mechanisms of resistance to BCR-ABL kinase inhibitors.

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1557-1565

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scholarly article

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10.18632/ONCOTARGET.692

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12

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3

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23238683

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3681494

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