ReviewJournal of experimental & clinical cancer research : CR2026
The double-edged sword role of tumor-associated macrophages: preventing or causing resistance to immunotherapy.
Review in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Peripheral T-Cell Receptor β Repertoire Dynamics Correlate with Response to Anti-PD-L1 Therapy in Non-Small Cell Lung Cancer.Cancers · 2026Article
- A double-edged sword: the role of macrophage pyroptosis-driven cytokine storm-mediated intercellular communication in tumor progression.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunotherapy has transformed cancer treatment, yet only a subset of patients achieves durable responses. Although macrophages play a key role in modulating immune response and could be used to enhance immunotherapy response, accumulating evidence highlights tumor-associated macrophages (TAMs) as both preventors or mediators of cancer, and its related therapies. TAMs contribute to resistance through multiple mechanisms, such as promoting T-cell exclusion, suppressing antitumor immunity via immunoregulatory cytokines, engaging metabolic checkpoints, and facilitating tumor angiogenesis. Clinical and single-cell transcriptomic studies further underscore the association between high TAM infiltration and poor immunotherapy outcomes. Emerging therapeutic strategies aim to reprogram, deplete, or block recruitment of TAMs, with several approaches currently being evaluated in early-phase clinical trials. This review summarizes the double-edged sword of TAMs M1-like proinflammatory or M2-like immunosuppressive states, in causing or preventing cancer. A deeper understanding of TAM heterogeneity and dynamics may enable the rational design of combination therapies and the development of predictive biomarkers to guide personalized immunotherapy.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.