Evidence map›Paper›PMID 31370337›Full record

ReviewCells2019

Metabolic Plasticity of Acute Myeloid Leukemia.

Johanna Kreitz, Christine Schönfeld, Marcel Seibert, Verena Stolp, Islam Alshamleh, Thomas Oellerich, Björn Steffen, Harald Schwalbe, Frank Schnütgen, Nina Kurrle and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

102 citing papers in PubMed, 155 citations in OpenAlex.

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42 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Johanna KreitzDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Christine SchönfeldDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Marcel SeibertDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Verena StolpDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Islam AlshamlehCenter for Biomolecular Magnetic Resonance, Institute of Organic Chemistry and Chemical Biology, Goethe-University, 60438 Frankfurt am Main, Germany.
Thomas OellerichDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Björn SteffenDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Harald SchwalbeGerman Cancer Consortium (DKTK) and DKFZ, 69120 Heidelberg, Germany.
Frank SchnütgenDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany.
Nina KurrleDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany. kurrle@med.uni-frankfurt.de.
Hubert ServeDepartment of Medicine 2, Hematology/Oncology, Goethe University, 60590 Frankfurt am Main, Germany. serve@em.uni-frankfurt.de.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Carbohydrate MetabolismEnergy MetabolismCitric Acid CycleGlycolysisHumansLeukemia, Myeloid, AcuteTumor Microenvironmentacute myeloid leukemiaaerobic glycolysisamino acidsdrug resistancefatty acidsleukemic stem cellsmetabolic plasticityoxidative phosphorylationredox homeostasisTCA cycle

Identifiers

PMID31370337
PMCPMC6721808
OpenAlexW2966025128

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.