ReviewFrontiers in immunology2026
Tumor-associated neutrophils in pancreatic ductal adenocarcinoma: mechanisms and therapeutic targeting.
Review in Frontiers in immunology, 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
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
3 citing papers in PubMed.
- The tumor microenvironment in pancreatic cancer: from composition to therapeutic targeting.Biochemical Society transactions · 2026Review
- Immunosuppressive cells as barriers to cancer therapy: mechanisms and emerging solutions.Frontiers in immunology · 2026Review
- Caught in the NET: A Review on the Emerging Role of Neutrophil Extracellular Traps in PDAC Development.Technology in cancer research & treatmentReview
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 (PDAC) remains one of the most lethal malignancies, characterized by profound therapeutic resistance and a 5-year survival rate below 10%. This prognosis is largely driven by a highly immunosuppressive tumor microenvironment (TME), in which tumor-associated neutrophils (TANs) serve as pivotal regulators. Upon recruitment to the TME, neutrophils undergo functional polarization into distinct phenotypes that either antagonize or facilitate tumor progression. This review synthesizes recent advances in PDAC research, delineating the ontogeny, subpopulation heterogeneity, and molecular mechanisms governing the pro- or anti-tumorigenic effects of TANs. We emphasize the regulatory crosstalk between TANs and the immune microenvironment, highlighting key signaling axes such as TGF-β and C-X-C chemokine receptor 2 (CXCR2) pathways. Furthermore, we evaluate TAN-targeted therapeutic strategies, categorizing them into recruitment inhibition, functional reprogramming, and immunosuppression disruption. Finally, we discuss translational challenges, including biomarker development and the shift from neutrophil depletion to functional reprogramming, offering perspectives for overcoming therapeutic resistance in PDAC.
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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.