Evidence map›Paper›PMID 42144527›Full record

ReviewCancer treatment and research2026

Cancer and Immune Cells: A Metabolic Battle in the Tumor Microenvironment.

Sam Pournezhad, Ramyar Azar, Farzad Taghizadeh-Hesary

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer treatment and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Sam Pournezhad *Marcus Stroke and Neuroscience Center, Grady Memorial Hospital, Atlanta, GA, USA.
Ramyar Azar *Iran University of Medical Sciences, Tehran, Iran.
Farzad Taghizadeh-HesaryBreast Cancer Research Center, Iran University of Medical Sciences, Tehran, Iran. taghizadeh_hesary.f@iums.ac.ir.ORCID https://orcid.org/0000-0002-6195-2203

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunometabolism has emerged as a critical field that links cellular energy regulation with immune function, including in the context of cancer. The tumor microenvironment (TME) is characterized by hypoxia, acidosis, and nutrient competition, all of which promote metabolic reprogramming in cancer cells while suppressing immune surveillance. Antitumor immune cells such as cytotoxic T lymphocytes, natural killer (NK) cells, and M1 macrophages rely on glycolysis and oxidative phosphorylation to sustain effector functions. In contrast, tumor-promoting cells, including regulatory T cells, myeloid-derived suppressor cells, and M2 macrophages, adopt oxidative metabolism and immunosuppressive pathways that reinforce immune escape. Cancer cells further evade immunity through immune checkpoint expression, reduced antigen presentation, secretion of suppressive cytokines, and mitochondrial hijacking, gaining bioenergetic superiority over immune cells. Current immunotherapies, such as checkpoint inhibitors, CAR-T cell therapy, cancer vaccines, and NK-cell-based therapies, have transformed cancer treatment but are often limited by TME-induced metabolic suppression. This chapter highlights the central role of metabolism in cancer-immune dynamics and introduces a novel therapeutic framework that integrates metabolic intervention with immune activation for improved cancer treatment outcomes.

Indexed as

NeoplasmsTumor MicroenvironmentAnimalsHumansImmunotherapyKiller Cells, NaturalMetabolic ReprogrammingCancerImmune systemImmunometabolismMitochondriaTumor microenvironment

Identifiers

What OpenQuestion holds

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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.