Actin cytoskeleton deregulation confers midostaurin resistance in FLT3-mutant acute myeloid leukemia

Garitano-Trojaola et al. used a combination of human acute myeloid leukemia (AML) cell lines and primary samples to show that RAC1-dependent actin cytoskeleton remodeling through BCL2 family plays a key role in resistance to the FLT3 inhibitor, Midostaurin in AML. They showed that by targeting RAC1...

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Auteurs principaux: Andoni Garitano-Trojaola, Ana Sancho, Ralph Götz, Patrick Eiring, Susanne Walz, Hardikkumar Jetani, Jesus Gil-Pulido, Matteo Claudio Da Via, Eva Teufel, Nadine Rhodes, Larissa Haertle, Estibaliz Arellano-Viera, Raoul Tibes, Andreas Rosenwald, Leo Rasche, Michael Hudecek, Markus Sauer, Jürgen Groll, Hermann Einsele, Sabrina Kraus, Martin K. Kortüm
Format: article
Langue:EN
Publié: Nature Portfolio 2021
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Accès en ligne:https://doaj.org/article/97fe6acc0451456bbe96d2d7eec2c3f6
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Résumé:Garitano-Trojaola et al. used a combination of human acute myeloid leukemia (AML) cell lines and primary samples to show that RAC1-dependent actin cytoskeleton remodeling through BCL2 family plays a key role in resistance to the FLT3 inhibitor, Midostaurin in AML. They showed that by targeting RAC1 and BCL2, Midostaurin resistance was diminished, which potentially paves the way for an innovate treatment approach for FLT3 mutant AML.