Evidence map›Paper›PMID 39625974›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Glutamine is critical for the maintenance of type 1 conventional dendritic cells in normal tissue and the tumor microenvironment.

Graham P Lobel, Nanumi Han, William A Molina Arocho, Michal Silber, Jason Shoush, Michael C Noji, Tsun Ki Jerrick To, Li Zhai, Nicholas P Lesner, M Celeste Simon and 1 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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  11. Glutamine is critical for the maintenance of type 1 conventional dendritic cells in normal tissue and the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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.

Graham P Lobel *Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Nanumi Han *Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
William A Molina ArochoDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Michal SilberDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Jason ShoushDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Michael C NojiDepartment of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.ORCID 0000-0002-6996-5367
Tsun Ki Jerrick ToDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Li ZhaiDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.
Nicholas P LesnerAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
M Celeste SimonAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Malay HaldarDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19014.

Funding

HEMATOLOGY CLINICAL RESEARCH TRAINING PROGRAMT32HL007439 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE F BRASS, PETER S KLEIN · 1985 to 2026
$17.1M
HEMATOPOIESIS TRAINING GRANTT32DK007780 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI TONG, WEI · 1999 to 2023
$6.7M
Regulation of antigen presenting cells in the tumor microenvironment by retinoic acidR37CA234027 · NCI · UNIVERSITY OF PENNSYLVANIA · PI HALDAR, MALAY · 2019 to 2025
$2.6M
Role of glutamine metabolism in Dendritic Cell DevelopmentR01DK138827 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HALDAR, MALAY · 2023 to 2025
$962k
The Role of Glutamine Metabolism in Monocyte-Derived Dendritic Cell Differentiation in the Soft-Tissue Sarcoma MicroenvironmentF30CA265069 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LOBEL, GRAHAM · 2021 to 2024
$153k
The role of branched-chain amino acid metabolism and hyperinsulinemia in pancreatic cancerF31CA261041 · NCI · UNIVERSITY OF PENNSYLVANIA · PI NOJI, MICHAEL · 2022 to 2024
$131k
Uncovering the function of EdnrB in perivascular macrophagesF31HL170590 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI William Molina · 2024 to 2026
$127k
Cancer Research Institute (CRI) STAR awardDamon Runyon Cancer Research Foundation (DRCRF) DRG2497HHS | NIH | National Cancer Institute (NCI) F30CA265069HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) F31HL170590HHS | NIH | NHLBI | Division of Intramural Research (DIR) T32 HL-07439HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) R01DK138827NCI NIH HHS F30 CA265069NCI NIH HHS F31 CA261041NCI NIH HHS R37 CA234027NHLBI NIH HHS F31 HL170590NHLBI NIH HHS T32 HL007439NIDDK NIH HHS R01 DK138827NIDDK NIH HHS T32 DK007780
6 · The paper itself

Abstract

Proliferating tumor cells take up glutamine for anabolic processes, engendering glutamine deficiency in the tumor microenvironment. How this might impact immune cells is not well understood. Using multiple mouse models of soft tissue sarcomas, glutamine antagonists, as well as genetic and pharmacological inhibition of glutamine utilization, we found that the number and frequency of conventional dendritic cells (cDCs) is dependent on microenvironmental glutamine levels. cDCs comprise two distinct subsets-cDC1s and cDC2s, with the former subset playing a critical role in antigen cross-presentation and tumor immunity. While both subsets show dependence on glutamine, cDC1s are particularly sensitive. Notably, glutamine antagonism did not reduce the frequency of DC precursors but decreased the proliferation and survival of cDC1s. Further studies suggest a role of the nutrient sensing mechanistic target of rapamycin (mTOR) signaling pathway in this process. Taken together, these findings uncover glutamine dependence of cDC1s that is coopted by tumors to escape immune responses.

Indexed as

Dendritic CellsGlutamineTOR Serine-Threonine KinasesTumor MicroenvironmentAnimalsCell ProliferationMiceMice, Inbred C57BLSignal TransductionGlutamineTOR Serine-Threonine Kinasesdendritic cellsglutaminetumor microenvironment

Identifiers

PMID39625974
PMCPMC11648871

What OpenQuestion holds

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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.