Evidence map›Paper›PMID 34239083›Full record

ReviewCellular & molecular immunology2022

The therapeutic implications of immunosuppressive tumor aerobic glycolysis.

Bradley I Reinfeld, W Kimryn Rathmell, Tae Kon Kim, Jeffrey C Rathmell

Abstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing 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

69 citing papers in PubMed.

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9 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

4 authors.

Bradley I ReinfeldDepartment of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.
W Kimryn RathmellDepartment of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.
Tae Kon KimDepartment of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.
Jeffrey C RathmellVanderbilt Center for Immunobiology, Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA. jeff.rathmell@vumc.org.ORCID http://orcid.org/0000-0002-4106-3396

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Medical Scientist Training ProgramT32GM152284 · NIGMS · VANDERBILT UNIVERSITY · PI Christopher S. Williams · 2024 to 2026
$4.8M
Metabolic Barriers to T Cell Activation in Clear Cell Renal Cell CarcinomaR01CA217987 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Jeffrey C Rathmell · 2018 to 2026
$4.3M
Metabolic Contributions of Individual Cellular Compartments to the Diversity of the Tumor Microenvironment in Renal Cell CarcinomaF30CA247202 · NCI · VANDERBILT UNIVERSITY · PI REINFELD, BRADLEY · 2021 to 2023
$107k
NCI NIH HHS F30 CA247202NCI NIH HHS R01 CA217987NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32 GM152284
6 · The paper itself

Abstract

In 2011, Hanahan and Weinberg added "Deregulating Cellular Energetics" and "Avoiding Immune Destruction" to the six previous hallmarks of cancer. Since this seminal paper, there has been a growing consensus that these new hallmarks are not mutually exclusive but rather interdependent. The following review summarizes how founding genetic events for tumorigenesis ultimately increase tumor cell glycolysis, which not only supports the metabolic demands of malignancy but also provides an immunoprotective niche, promoting malignant cell proliferation, maintenance and progression. The mechanisms by which altered metabolism contributes to immune impairment are multifactorial: (1) the metabolic demands of proliferating tumor cells and activated immune cells are similar, thus creating a situation where immune cells may be in competition for key nutrients; (2) the metabolic byproducts of aerobic glycolysis directly inhibit antitumor immunity while promoting a regulatory immune phenotype; and (3) the gene programs associated with the upregulation of glycolysis also result in the generation of immunosuppressive cytokines and metabolites. From this perspective, we shed light on important considerations for the development of new classes of agents targeting cancer metabolism. These types of therapies can impair tumor growth but also pose a significant risk of stifling antitumor immunity.

Indexed as

NeoplasmsCitric Acid CycleGlycolysisHumanscancerglycolysisimmunologymetabolism

Identifiers

PMID34239083
PMCPMC8752729

What OpenQuestion holds

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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.