ReviewExperimental & molecular medicine2026
Metabolic adaptations of immunosuppressive cells in cancer: mechanisms and therapeutic targets.
Review in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed.
- Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Clinical and experimental medicine · 2026Review
- Nanoplatform-Mediated Remodeling of the Immune Microenvironment in Renal Cell Carcinoma.International journal of nanomedicine · 2026Review
- Tumor-associated macrophages in gastric cancer peritoneal metastasis: orchestrating immune evasion, niche remodeling, and therapeutic resistance.Frontiers in immunology · 2026Review
- Metabolic licensing and restriction of innate immunity in the tumor microenvironment.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The tumor microenvironment harbors diverse immunosuppressive cell populations-including regulatory T cells, myeloid-derived suppressor cells, tumor-associated macrophages and other tolerogenic subsets-that drive immune evasion and therapeutic resistance. These cells are metabolically reprogrammed to sustain their suppressive function and survive under conditions of hypoxia, nutrient deprivation and oxidative stress. Importantly, their metabolic activity not only supports their own fitness but also creates a hostile environment that antagonizes effector T and natural killer cells by depleting essential nutrients, generating inhibitory metabolites, and altering signaling thresholds. This immunometabolic competition reinforces immune dysfunction and limits the efficacy of checkpoint blockade and adoptive cell therapies. Here we delineate the immunosuppressive cell types within the TME, their key metabolic adaptations and the mechanisms by which they suppress antitumor immunity. Finally, we discuss therapeutic strategies aimed at disrupting these metabolic programs to remodel the TME and enhance the success of current and next-generation immunotherapies. Collectively, understanding the metabolic crosstalk between suppressive and effector immune cells will provide new opportunities to design precision metabolic interventions and improve durable responses to cancer immunotherapy.
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Registered trials
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.