Increased Proliferation Induced by Constitutive Activation of the Src-Kinase Lyn and Aberrant mTOR Signaling in AML Is Abrogated by the EGFR-Inhibitor Erlotinib.

Simone Boehrer; Lorenzo Galluzzi; Lionel Adès; Celine Fouassier; Claude Gardin; Pierre Fenaux; Guido Guido Kroemer

doi:10.1182/blood.v114.22.3813.3813

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Increased Proliferation Induced by Constitutive Activation of the Src-Kinase Lyn and Aberrant mTOR Signaling in AML Is Abrogated by the EGFR-Inhibitor Erlotinib.

Discussion(0)

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Erlotinib antagonizes constitutive activation of SRC family kinases and mTOR in acute myeloid leukemia

Potentiation of Apoptosis in MDS/AML by Combination of Azacitidine and the EGFR-Tyrosine Kinase Inhibitor (TKI) erlotinib

P039 The EGFR-inhibitor erlotinib exhibits various off-target effects in MDS and AML

Erlotinib Antagonizes Efflux Via ABC Transporters and Decreases P-Gp Cell Surface Expression by Inhibiting SRC Kinase and mTOR Pathways in Acute Myeloid Leukemia (AML)

The EGFR-Inhibitor Erlotinib Induces Differentiation, Cell Cycle Arrest and Apoptosis in EGFR-Negative Cells of MDS and AML.