Evidence map›Paper›PMID 42284139›Full record

ArticleCell reports2026

Cancer-associated fibroblast subtypes differentially modulate natural killer cells in cancer.

Leonor Nunes Rodrigues, Hafsa Munir, Ibone Thate Arrazola, Matthias M Gaida, Christoph Eckert, Jerome Boulanger, Ana C F Ferreira, Andrew N J McKenzie, Jacqueline D Shields

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Leonor Nunes RodriguesMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, UK.
Hafsa MunirMRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, UK; Helmholtz Institute for Translational Oncology Mainz (HI-TRON Mainz) - a Helmholtz Institute of the DKFZ, Mainz, Germany; German Cancer Research Centre (DKFZ), Division of Dermal Oncoimmunology, Heidelberg, Germany.
Ibone Thate ArrazolaHelmholtz Institute for Translational Oncology Mainz (HI-TRON Mainz) - a Helmholtz Institute of the DKFZ, Mainz, Germany; German Cancer Research Centre (DKFZ), Division of Dermal Oncoimmunology, Heidelberg, Germany.
Matthias M GaidaInstitute of Pathology, University Medical Center Mainz, JGU-Mainz 55131 Mainz, Germany; TRON, Translational Oncology at the University Medical Center, JGU-Mainz 55131 Mainz, Germany; Research Center for Immunotherapy, University Medical Center Mainz, JGU-Mainz 55131 Mainz, Germany.
Christoph EckertInstitute of Pathology, University Medical Center Mainz, JGU-Mainz 55131 Mainz, Germany; TRON, Translational Oncology at the University Medical Center, JGU-Mainz 55131 Mainz, Germany.
Jerome BoulangerMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Ana C F FerreiraMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Andrew N J McKenzieMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK. Electronic address: anm@mrc-lmb.cam.ac.uk.
Jacqueline D ShieldsMRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, UK; Comprehensive Cancer Centre, Kings College London, London, UK; Centre for Cancer Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK. Electronic address: jacqueline.shields@nottingham.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells are cytotoxic innate lymphoid cells which directly kill tumor cells, thus represent an attractive target for immunotherapy. However, NK cells face immunosuppression in the tumor microenvironment (TME), rendering them dysfunctional. While cancer-associated fibroblasts (CAFs) represent an abundant, heterogeneous component of pancreatic ductal adenocarcinoma (PDAC), their interplay with NK cells is largely understudied. Analyzing human samples and employing mouse models of PDAC and functional assays, we observed that intratumoral NK cells are immature, and TGF-β driven myofibroblastic (my)CAFs are strong NK suppressors, in contrast to inflammatory (i)CAF. Furthermore, myCAF-enriched tumor areas excluded NK cells, consistent with their reduced capacity to attract NK cells. Pancreatic CAFs in general reduced NK cell cytotoxicity by direct contact and via soluble factors, including prostaglandin E2 (PGE2). This work reveals distinct and overlapping roles of CAF subpopulations on NK cell functions, suggesting that overcoming CAF-imposed barriers to NK cytotoxicity and tumor infiltration is essential to unleash their anti-tumoral properties.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalKiller Cells, NaturalPancreatic NeoplasmsAnimalsCell Line, TumorDinoprostoneHumansMiceMice, Inbred C57BLTumor MicroenvironmentDinoprostoneCAFCP: cancerCP: immunologyfibroblastsNK cellsPDACPGE2tumor microenvironment

Identifiers

PMID42284139
PMCPMC7619464

What OpenQuestion holds

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Registered trials

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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.