PMID: 19934662Nov 26, 2009Paper

Targeting translation in acute myeloid leukemia: a new paradigm for therapy?

Cell Cycle
Jerome TamburiniDidier Bouscary

Abstract

The mammalian Target Of Rapamycin Complex 1 (mTORC1) pathway is commonly activated in cancer cells including acute myeloid leukemia (AML) and has been designed as a major target for cancer therapy. However, the efficacy of rapalogs (mTORC1 inhibitors) is limited in AML, due to the feedback activation of PI3K or ERK signaling pathways upon mTORC1 inhibition, which pathways should be simultaneously targeted to enhance the anti-leukemic activity of rapalogs. Moreover, the mRNA translation process is mTORC1-independent in AML, although markedly contributing to oncogenesis in this disease, and this also strongly participates to rapalogs resistance. Translation inhibition could be achieved by directly targeting the translation initiating complex using the 4EGI-1 compound, anti-eIF4E antisense oligonucleotides or the antiviral drug ribavirin or by second generation mTOR inhibitors (TORkinhibs). These new approaches represent promising perspectives for AML therapy that should have clinical development in the future.

Citations

Jul 29, 2010·Molecular Pharmacology·Jessica K AltmanLeonidas C Platanias
Jun 14, 2014·Journal of Translational Medicine·Himalee SabnisKevin D Bunting
Jun 13, 2013·Expert Opinion on Therapeutic Targets·Camilla EvangelistiAlberto M Martelli
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Jun 13, 2012·Expert Opinion on Therapeutic Targets·Alberto M MartelliJames A McCubrey
Feb 14, 2012·Clinics in Geriatric Medicine·Anthony MatoAndre Goy
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Jun 28, 2014·International Journal of Oncology·Camilla EvangelistiAlberto M Martelli
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Mar 5, 2016·Molecular Cancer Therapeutics·Shirong LiSuzanne Lentzsch

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