Metabolic Plasticity of Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is one of the most common and life-threatening leukemias. A highly diverse and flexible metabolism contributes to the aggressiveness of the disease that is still difficult to treat. By using different sources of nutrients for energy and biomass supply, AML cells gain met...

Full description

Saved in:
Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2019-07, Vol.8 (8), p.805
Main Authors: Kreitz, Johanna, Schönfeld, Christine, Seibert, Marcel, Stolp, Verena, Alshamleh, Islam, Oellerich, Thomas, Steffen, Björn, Schwalbe, Harald, Schnütgen, Frank, Kurrle, Nina, Serve, Hubert
Format: Article
Language:English
Subjects:
Acute myeloid leukemia
aerobic glycolysis
amino acids
Bone marrow
Cancer therapies
Carbohydrate Metabolism
Citric Acid Cycle
Cloning
Disease
Drug resistance
Energy Metabolism
Environmental changes
Enzymes
Epigenetics
Fatty acids
Glucose
Glutamine
Glycolysis
Homeostasis
Humans
Kinases
Leukemia
Leukemia, Myeloid, Acute - metabolism
leukemic stem cells
Lipid metabolism
Medical prognosis
metabolic plasticity
Metabolism
Metabolites
Mutation
Myeloid leukemia
oxidative phosphorylation
Plasticity
redox homeostasis
Review
Stem cells
TCA cycle
Tricarboxylic acid cycle
Tumor Microenvironment
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Acute myeloid leukemia (AML) is one of the most common and life-threatening leukemias. A highly diverse and flexible metabolism contributes to the aggressiveness of the disease that is still difficult to treat. By using different sources of nutrients for energy and biomass supply, AML cells gain metabolic plasticity and rapidly outcompete normal hematopoietic cells. This review aims to decipher the diverse metabolic strategies and the underlying oncogenic and environmental changes that sustain continuous growth, mediate redox homeostasis and induce drug resistance in AML. We revisit Warburg's hypothesis and illustrate the role of glucose as a provider of cellular building blocks rather than as a supplier of the tricarboxylic acid (TCA) cycle for energy production. We discuss how the diversity of fuels for the TCA cycle, including glutamine and fatty acids, contributes to the metabolic plasticity of the disease and highlight the roles of amino acids and lipids in AML metabolism. Furthermore, we point out the potential of the different metabolic effectors to be used as novel therapeutic targets.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells8080805