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Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia

Metabolic reprogramming is a common cancer cell phenotype as it sustains growth and proliferation. Targeting metabolic activities offers a wide range of therapeutic possibilities which are applicable to acute myeloid leukemia (AML). Indeed, in addition to the IDH1/2-mutated AML model which establish...

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Autores principales: Chapuis, Nicolas, Poulain, Laury, Birsen, Rudy, Tamburini, Jerome, Bouscary, Didier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540604/
https://www.ncbi.nlm.nih.gov/pubmed/31192118
http://dx.doi.org/10.3389/fonc.2019.00405
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author Chapuis, Nicolas
Poulain, Laury
Birsen, Rudy
Tamburini, Jerome
Bouscary, Didier
author_facet Chapuis, Nicolas
Poulain, Laury
Birsen, Rudy
Tamburini, Jerome
Bouscary, Didier
author_sort Chapuis, Nicolas
collection PubMed
description Metabolic reprogramming is a common cancer cell phenotype as it sustains growth and proliferation. Targeting metabolic activities offers a wide range of therapeutic possibilities which are applicable to acute myeloid leukemia (AML). Indeed, in addition to the IDH1/2-mutated AML model which established the proof-of-concept for specifically targeting metabolic adaptations in AML, several recent reports have expanded the scope of such strategies in these diseases. This review highlights recent findings on metabolic deregulation in AML and summarizes their implications in leukemogenesis.
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spelling pubmed-65406042019-06-12 Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia Chapuis, Nicolas Poulain, Laury Birsen, Rudy Tamburini, Jerome Bouscary, Didier Front Oncol Oncology Metabolic reprogramming is a common cancer cell phenotype as it sustains growth and proliferation. Targeting metabolic activities offers a wide range of therapeutic possibilities which are applicable to acute myeloid leukemia (AML). Indeed, in addition to the IDH1/2-mutated AML model which established the proof-of-concept for specifically targeting metabolic adaptations in AML, several recent reports have expanded the scope of such strategies in these diseases. This review highlights recent findings on metabolic deregulation in AML and summarizes their implications in leukemogenesis. Frontiers Media S.A. 2019-05-22 /pmc/articles/PMC6540604/ /pubmed/31192118 http://dx.doi.org/10.3389/fonc.2019.00405 Text en Copyright © 2019 Chapuis, Poulain, Birsen, Tamburini and Bouscary. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Chapuis, Nicolas
Poulain, Laury
Birsen, Rudy
Tamburini, Jerome
Bouscary, Didier
Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title_full Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title_fullStr Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title_full_unstemmed Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title_short Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia
title_sort rationale for targeting deregulated metabolic pathways as a therapeutic strategy in acute myeloid leukemia
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540604/
https://www.ncbi.nlm.nih.gov/pubmed/31192118
http://dx.doi.org/10.3389/fonc.2019.00405
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