Evidence map›Paper›PMID 40420205›Full record

ArticleCancer & metabolism2025

Impact of physiological media on acute myeloid leukemia bioenergetics and cell proliferation.

Brett R Chrest, McLane M Montgomery, Raphael T Aruleba, Polina Krassovskaia, Emely A Pacheco, James T Hagen, Kayla J Vandiver, Kang Tung, Molly K Alexander, Nicholas C Williamson and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

27 authors.

Brett R Chrest *Department of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
McLane M Montgomery *Department of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
Raphael T ArulebaDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
Polina KrassovskaiaDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
Emely A PachecoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
James T HagenDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Kayla J VandiverDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Kang TungDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Molly K AlexanderDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Nicholas C WilliamsonDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Joshua G TaylorDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Riley N BessettiEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Heather A BelcherEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Filip JevtovicHuman Performance Laboratory, Department of Kinesiology, East Carolina University, Greenville, NC, USA.
Zoe S TerwilligerDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Everett C MinchewDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Tonya N ZeczyckiDepartment of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Linda MayHuman Performance Laboratory, Department of Kinesiology, East Carolina University, Greenville, NC, USA.
Nicholas T BroskeyEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Christopher B GeyerEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Karen LitwaEast Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Espen E SpangenburgDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Johanna L HannanDepartment of Urology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Jessica M EllisDepartment of Physiology, East Carolina University, Greenville, NC, USA.
Joseph M McClungDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
P Darrell NeuferDepartment of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Kelsey H Fisher-WellmanDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA. kfisherw@wakehealth.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing emphasis has been placed on improving the physiological relevance of cell culture media with formulations such as Human Plasma-Like Medium (HPLM). Given that shifts in mitochondrial metabolism and nutrient use are emerging as anti-cancer targets, the present study sought to investigate the impact of culture media formulation on mitochondrial bioenergetics and cancer cell growth. To do this, we used acute myeloid leukemia (AML) cells and compared acute and chronic effects of HPLM versus different supraphysiological medias. The AML mitochondrial phenotype was largely unaffected by exposure to either physiological or supraphysiological medias, establishing that the key features of AML mitochondria remain phenotypically stable under diverse nutrient conditions and proliferation rates. Both acute and chronic culturing in HPLM slowed AML cell proliferation. However, merely identifying and supplementing single nutrients that were deficient in HPLM did not improve proliferation and was not sufficient to pinpoint actionable fuel preferences. Transferring cells back to native Iscove's Modified Dulbecco's Medium (IMDM) media immediately restored the proliferative phenotype, suggesting responsiveness to the entirety of the nutrient environment. Supraphysiological culture medias other than IMDM were all characterized by slower proliferation; however, none were associated with changes in cell viability, demonstrating that the native culture medium is optimal if the experimental aim is maximal growth. Despite Dulbecco's Modified Eagle Medium (DMEM) being similar in nutrient composition to IMDM and categorized as supraphysiological, both acute and chronic culturing in DMEM resulted in slower growth, akin to what was observed with HPLM. Altogether, independent of growth, AML mitochondria remain largely unperturbed by changes in the culture media, and rather than specific nutrients or physiological relevance, AML cell proliferation is influenced by the complete nutrient profile.

Identifiers

PMID40420205
PMCPMC12105319

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.