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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: 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
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
Acceso en línea:https://doaj.org/article/97fe6acc0451456bbe96d2d7eec2c3f6
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
Descripción
Sumario: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.