Evidence map›Paper›PMID 38490211›Full record

ArticleCell metabolism2024

Acetyl-CoA carboxylase obstructs CD8

Elizabeth G Hunt, Katie E Hurst, Brian P Riesenberg, Andrew S Kennedy, Evelyn J Gandy, Alex M Andrews, Coral Del Mar Alicea Pauneto, Lauren E Ball, Emily D Wallace, Peng Gao and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
24.8field-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

81 citing papers in PubMed, 87 citations in OpenAlex.

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21 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

14 authors at 3 institutions in 1 country.

Elizabeth G HuntImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Cell Biology & Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Katie E HurstImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Brian P RiesenbergImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Andrew S KennedyImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Cell Biology & Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Evelyn J GandyImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Alex M AndrewsDepartment of Microbiology & Immunology, Medical University of South Carolina, Charleston, SC 29425, USA.
Coral Del Mar Alicea PaunetoImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Lauren E BallDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC 29425, USA.
Emily D WallaceDepartment of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Peng GaoDepartment of Medicine, Metabolomics Core Facility, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Jeremy MeierImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Microbiology & Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
John J SerodyImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Microbiology & Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Michael F ColemanDepartment of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Jessica E ThaxtonImmunotherapy Program, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA; Department of Cell Biology & Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA. Electronic address: jess_thaxton@med.unc.edu.
University of North Carolina at Chapel Hill · USMedical University of South Carolina · USNorthwestern University · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI John J Lemasters · 2009 to 2026
$42.7M
CANCER CELL BIOLOGY TRAINING PROGRAMT32CA071341 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHANNING J. DER, Yuliya Pylayeva-Gupta · 1996 to 2026
$5.0M
Targeting Chronic ER Stress in T Cells to Improve Cancer ImmunotherapyR01CA244361 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI THAXTON, JESSICA E · 2020 to 2024
$1.9M
Expoitation of ER Stress Induced Immune Dysfunction to Improve ImmunotherapyR01CA248359 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI THAXTON, JESSICA E · 2020 to 2024
$1.7M
Orbitrap Fusion Lumos ETD Mass SpectrometerS10OD025126 · OD · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BALL, LAUREN ELIZABETH · 2018 to 2018
$991k
NCI NIH HHS P30 CA016086NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA244361NCI NIH HHS R01 CA248359NCI NIH HHS T32 CA071341NIH HHS S10 OD025126
6 · The paper itself

Abstract

The solid tumor microenvironment (TME) imprints a compromised metabolic state in tumor-infiltrating T cells (TILs), hallmarked by the inability to maintain effective energy synthesis for antitumor function and survival. T cells in the TME must catabolize lipids via mitochondrial fatty acid oxidation (FAO) to supply energy in nutrient stress, and it is established that T cells enriched in FAO are adept at cancer control. However, endogenous TILs and unmodified cellular therapy products fail to sustain bioenergetics in tumors. We reveal that the solid TME imposes perpetual acetyl-coenzyme A (CoA) carboxylase (ACC) activity, invoking lipid biogenesis and storage in TILs that opposes FAO. Using metabolic, lipidomic, and confocal imaging strategies, we find that restricting ACC rewires T cell metabolism, enabling energy maintenance in TME stress. Limiting ACC activity potentiates a gene and phenotypic program indicative of T cell longevity, engendering T cells with increased survival and polyfunctionality, which sustains cancer control.

Indexed as

Acetyl-CoA CarboxylaseCD8-Positive T-LymphocytesLipid MetabolismTumor MicroenvironmentAnimalsCell Line, TumorFatty AcidsFemaleHumansLymphocytes, Tumor-InfiltratingMiceMice, Inbred C57BLMitochondriaAcetyl-CoA CarboxylaseFatty Acidsendoplasmic reticulumimmunotherapylipidmetabolismmitochondriaT celltumor microenvironment

Identifiers

PMID38490211
PMCPMC12010431
OpenAlexW4392802359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.