ReviewWorld journal of clinical oncology2026
Immunosuppressive tumor microenvironment shape pancreatic cancer unresponsive to current immunotherapies.
Review in World journal of clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- The Association Between Neutrophil-to-Lymphocyte Ratio and Histological Tumor Differentiation in Solid Malignancies: A Systematic Review.Diagnostics (Basel, Switzerland) · 2026Review
- Deciphering immunosuppressive niches by spatial single-cell proteomics: spatial interaction networks and translational opportunities.Frontiers in immunology · 2026Review
- Immunosuppressive cells as barriers to cancer therapy: mechanisms and emerging solutions.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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma remains largely refractory to current immunotherapies due to a profoundly immunosuppressive tumor microenvironment dominated by regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages (TAMs). These cells form a coordinated network that suppresses cytotoxic T lymphocytes and fosters tumor progression. Key mechanisms include Tregs secreting inhibitory cytokines like transforming growth factor β and interleukin-10, and upregulating immune checkpoints such as cytotoxic T-lymphocyte-associated protein 4 and programmed death 1. MDSCs deplete essential nutrients like arginine and generate reactive oxygen species, while TAMs polarized to an M2 phenotype produce chemokines including C-C motif chemokine ligand 2 and C-X-C motif chemokine ligand 12, which recruit more suppressive cells. Single-cell transcriptomic studies have uncovered prognostically relevant cellular subsets, such as caspase-4-high Tregs, highlighting this heterogeneity. Reciprocal signaling
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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.