Modelling ponatinib resistance in tyrosine kinase inhibitor-naïve and dasatinib resistant + cell lines

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Modelling ponatinib resistance in tyrosine kinase inhibitor-naïve and dasatinib resistant + cell lines

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im Oktober 2018 veröffentlichter wissenschaftlicher Artikel

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scientific article published on 05 October 2018

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wetenschappelijk artikel

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наукова стаття, опублікована в жовтні 2018

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name

Modelling ponatinib resistance ...... satinib resistant + cell lines

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Modelling ponatinib resistance ...... satinib resistant + cell lines

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Modelling ponatinib resistance ...... satinib resistant + cell lines

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Modelling ponatinib resistance ...... satinib resistant + cell lines

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Modelling ponatinib resistance ...... satinib resistant + cell lines

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Modelling ponatinib resistance ...... satinib resistant + cell lines

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P1476

Modelling ponatinib resistance ...... resistant BCR-ABL1+ cell lines

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Chung Hoow Kok

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Jennifer Anne McLean

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Jueqiong Wang

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Liu Lu

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Timothy Peter Hughes

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Verity Ann Saunders

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P2860

AXL mediates resistance to PI3Kα inhibition by activating the EGFR/PKC/mTOR axis in head and neck and esophageal squamous cell carcinomas

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

Ponatinib is a pan-BCR-ABL kinase inhibitor: MD simulations and SIE study

Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.

Axl is an essential epithelial-to-mesenchymal transition-induced regulator of breast cancer metastasis and patient survival.

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

Active transport of imatinib into and out of cells: implications for drug resistance.

The novel receptor tyrosine kinase Axl is constitutively active in B-cell chronic lymphocytic leukemia and acts as a docking site of nonreceptor kinases: implications for therapy.

Axl phosphorylates Elmo scaffold proteins to promote Rac activation and cell invasion.

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34735-34747

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scholarly article

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10.18632/ONCOTARGET.26187

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English

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Deborah L. White

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2018-10-05T00:00:00Z

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30410673

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6205183

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