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• W1662899804 abstract "Fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) is frequently detected in acute myeloid leukemia (AML) patients and is associated with a dismal long-term prognosis. FLT3 tyrosine kinase inhibitors provide short-term disease control, but relapse invariably occurs within months. Pim protein kinases are oncogenic FLT3-ITD targets expressed in AML cells. We show that increased Pim kinase expression is found in relapse samples from AML patients treated with FLT3 inhibitors. Ectopic Pim-2 expression induces resistance to FLT3 inhibition in both FLT3-ITD-induced myeloproliferative neoplasm and AML models in mice. Strikingly, we found that Pim kinases govern FLT3-ITD signaling and that their pharmacological or genetic inhibition restores cell sensitivity to FLT3 inhibitors. Finally, dual inhibition of FLT3 and Pim kinases eradicates FLT3-ITD(+) cells including primary AML cells. Concomitant Pim and FLT3 inhibition represents a promising new avenue for AML therapy." @default.
• W1662899804 created "2016-06-24" @default.
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• W1662899804 date "2015-09-04" @default.
• W1662899804 modified "2023-10-14" @default.
• W1662899804 title "Pim kinases modulate resistance to FLT3 tyrosine kinase inhibitors in FLT3-ITD acute myeloid leukemia" @default.
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• W1662899804 doi "https://doi.org/10.1126/sciadv.1500221" @default.
• W1662899804 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4643770" @default.
• W1662899804 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26601252" @default.
• W1662899804 hasPublicationYear "2015" @default.
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