Evidence map›Paper›PMID 36052997›Full record

ArticleeLife2022

Crosstalk between AML and stromal cells triggers acetate secretion through the metabolic rewiring of stromal cells.

Nuria Vilaplana-Lopera, Vincent Cuminetti, Ruba Almaghrabi, Grigorios Papatzikas, Ashok Kumar Rout, Mark Jeeves, Elena González, Yara Alyahyawi, Alan Cunningham, Ayşegül Erdem and 9 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  5. [Gender differences in acylcarnitine metabolism among patients with depression disorder].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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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

19 authors at 7 institutions in 5 countries.

Nuria Vilaplana-LoperaInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID https://orcid.org/0000-0002-3156-9908
Vincent Cuminetti *Stem Cells, Ageing and Cancer Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT - The Arctic University of Norway, Tromso, Norway.ORCID https://orcid.org/0000-0001-8396-710X
Ruba Almaghrabi *Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Grigorios Papatzikas *Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID https://orcid.org/0000-0002-0163-4174
Ashok Kumar RoutInstitute of Chemistry and Metabolomics, University of Lübeck, Lübeck, Germany.
Mark JeevesInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID https://orcid.org/0000-0001-9736-0990
Elena GonzálezInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Yara AlyahyawiInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Alan CunninghamDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Ayşegül ErdemDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Frank SchnütgenDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe University Frankfurt, Frankfurt, Germany.
Manoj RaghavanInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Sandeep PotluriInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Jean-Baptiste CazierInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Jan Jacob SchuringaDepartment of Experimental Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.ORCID https://orcid.org/0000-0001-8452-8555
Michelle A C ReedInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.
Lorena ArranzStem Cells, Ageing and Cancer Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT - The Arctic University of Norway, Tromso, Norway.ORCID https://orcid.org/0000-0002-5896-4238
Ulrich L GüntherInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID https://orcid.org/0000-0001-9840-5943
Paloma GarciaInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID https://orcid.org/0000-0001-5582-8575
University of Birmingham · GBUniversity Medical Center Groningen · NLUiT The Arctic University of Norway · NOUniversity Hospitals Birmingham NHS Foundation Trust · GBAl Baha University · SAGoethe University Frankfurt · DEUniversity of Lübeck · DE

Funding

Medical Research Council MR/P019609/1Wellcome Trust 208400/Z/17/Z
6 · The paper itself

Abstract

Acute myeloid leukaemia (AML) cells interact and modulate components of their surrounding microenvironment into their own benefit. Stromal cells have been shown to support AML survival and progression through various mechanisms. Nonetheless, whether AML cells could establish beneficial metabolic interactions with stromal cells is underexplored. By using a combination of human AML cell lines and AML patient samples together with mouse stromal cells and a MLL-AF9 mouse model, here we identify a novel metabolic crosstalk between AML and stromal cells where AML cells prompt stromal cells to secrete acetate for their own consumption to feed the tricarboxylic acid cycle (TCA) and lipid biosynthesis. By performing transcriptome analysis and tracer-based metabolic NMR analysis, we observe that stromal cells present a higher rate of glycolysis when co-cultured with AML cells. We also find that acetate in stromal cells is derived from pyruvate via chemical conversion under the influence of reactive oxygen species (ROS) following ROS transfer from AML to stromal cells via gap junctions. Overall, we present a unique metabolic communication between AML and stromal cells and propose two different molecular targets, ACSS2 and gap junctions, that could potentially be exploited for adjuvant therapy.

Indexed as

Leukemia, Myeloid, AcuteAcetatesAnimalsHumansLipidsMicePyruvatesReactive Oxygen SpeciesSignal TransductionStromal CellsTumor MicroenvironmentAcetatesLipidsPyruvatesReactive Oxygen Speciesacute myeloid leukaemiabiochemistrycancer biologychemical biologyhumanmetabolismmicroenvironmentmousenuclear magnetic resonance

Identifiers

PMID36052997
PMCPMC9477493
OpenAlexW4294287378

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.