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FLT3-ITD cooperates with Rac1 to modulate the sensitivity of leukemic cells to chemotherapeutic agents via regulation of DNA repair pathways

Acute myeloid leukemia (AML) is an aggressive hematologic neoplasm, and patients with an internal tandem duplication (ITD) mutation of the FMS-like tyrosine kinase-3 (FLT3) receptor gene have a poor prognosis. FLT3-ITD interacts with DOCK2, a G effector protein that activates Rac1/2. Previously, we...

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Bibliografski detalji
Izdano u:Haematologica
Glavni autori: Wu, Min, Li, Li, Hamaker, Max, Small, Donald, Duffield, Amy S.
Format: Artigo
Jezik:Inglês
Izdano: Ferrata Storti Foundation 2019
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Online pristup:https://ncbi.nlm.nih.gov/pmc/articles/PMC6959181/
https://ncbi.nlm.nih.gov/pubmed/30975911
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3324/haematol.2018.208843
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