ReviewBiomarker research2026
Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.
Review in Biomarker research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Spatial ecotype in tumor immune exclusion: from spatial architecture to therapeutic strategies.Molecular cancer · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to cancer immunotherapy markedly limits clinical benefit, and neutrophil extracellular traps (NETs) have emerged as critical mediators in shaping the immunosuppressive tumor microenvironment. The molecular components of NETs, including cell-free DNA, myeloperoxidase (MPO)-DNA complexes, and citrullinated histones (H3Cit)-have demonstrated significant clinical utility as diagnostic indicators and prognostic biomarkers for predicting disease progression and immunotherapy outcomes. Regulated by a complex network of tumor-derived signals and exosomes, NETs form dense physical barriers and promote T-cell exhaustion. This review elucidates the heterogeneity of NET formation and dissects the core mechanisms by which NETs mediate therapeutic resistance along two interrelated dimensions: spatial physical exclusion and biological functional modulation. Furthermore, we synthesize emerging strategies to target NETs-including inhibition of their formation, degradation of established barriers, and blockade of downstream interactions-with the aim of providing conceptual frameworks and translational directions for reshaping anti-tumor immunity and overcoming immunotherapy resistance.
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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.