Evidence map›Paper›PMID 40369538›Full record

ArticleCancer cell international2025

BCR::ABL1 expression in chronic myeloid leukemia cells in low oxygen is regulated by glutamine via CD36-mediated fatty acid uptake.

Caterina Mancini, Giulio Menegazzi, Silvia Peppicelli, Giampaolo Versienti, Daniele Guasti, Giuseppe Pieraccini, Elisabetta Rovida, Matteo Lulli, Laura Papucci, Persio Dello Sbarba and 1 more

Abstract read
In one paragraph

Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
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.

Caterina ManciniDepartment of Experimental and Clinical Medicine, Università degli Studi di Firenze, Florence, Italy.
Giulio MenegazziDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Silvia PeppicelliDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Giampaolo VersientiDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Daniele GuastiDepartment of Experimental and Clinical Medicine, Università degli Studi di Firenze, Florence, Italy.
Giuseppe PieracciniCISM Mass Spectrometry Center, Università degli Studi di Firenze, Florence, Italy.
Elisabetta RovidaDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Matteo LulliDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Laura PapucciDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Persio Dello SbarbaDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy. persio.dellosbarba@unifi.it.
Alessio BiagioniDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio", Università degli Studi di Firenze, Florence, Italy. alessio.biagioni@unifi.it.

Funding

Fondazione AIRC per la ricerca sul cancro ETS IG23607/2019
6 · The paper itself

Abstract

backgroundChronic myeloid leukemia (CML) is influenced by microenvironmental nutrients, glucose (Glc), and glutamine (Gln) which regulate cell proliferation, viability, and the expression of the driver oncoprotein (BCR::ABL1).

resultsOur study revealed that Glc, while partially supporting alone cell growth in normoxia, is essential in low oxygen conditions, whereas Gln is ineffective. Under low oxygen, Gln reduced oxidative respiratory activity while enhancing glycolysis. In these conditions, fatty acid (FA) metabolism becomes crucial, as evidenced by increased lipid droplets (LD) accumulation when Glc was absent. Gln, in particular, drives CD36-mediated FA uptake, suppressing the BCR::ABL1 oncoprotein and facilitating cell survival. By co-culturing leukemia cells with adipocytes, one of the main bone marrow (BM) cell components, we observed an enhanced FA release, suggesting a link between FA, microenvironmental BM cells, and the maintenance of leukemic stem cells (LSC).

methodsK562 and KCL22 cell lines were subjected to Glc and/or Gln deprivation under hypoxic conditions (96 h at 0.1% O

conclusionsThese findings underscore the central role of FA in the regulation of the LSC compartment of CML, highlighting the importance of Gln in facilitating CML cell survival under restrictive metabolic conditions and preparing the cell population for expansion upon the release of these restrictions.

Indexed as

BCR:ABL1Chronic myeloid leukemiaFatty acidsHypoxia

Identifiers

PMID40369538
PMCPMC12080266

What OpenQuestion holds

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Registered trials

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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.