Evidence map›Paper›PMID 34204306›Full record

ReviewBiomolecules2021

Immune Cell Modulation of the Extracellular Matrix Contributes to the Pathogenesis of Pancreatic Cancer.

Ramiz S Ahmad, Timothy D Eubank, Slawomir Lukomski, Brian A Boone

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 6% of its field
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

34 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  4. Observational
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  7. Article
  8. GlycoChat Uncovers Glycan-Lectin Circuits in the Tumor Microenvironment of Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  9. Modulating tumor mechanics and vascular barriers to enhance chemotherapy efficacy in pancreatic tumors and melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
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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

4 authors at 1 institution in 1 country.

Ramiz S AhmadDepartment of Surgery, West Virginia University, Morgantown, WV 26506, USA.ORCID 0000-0002-2856-3927
Timothy D EubankDepartment of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, WV 26506, USA.ORCID 0000-0002-8225-7824
Slawomir LukomskiDepartment of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, WV 26506, USA.ORCID 0000-0002-5159-1838
Brian A BooneDepartment of Surgery, West Virginia University, Morgantown, WV 26506, USA.
West Virginia University · US

Funding

NIH HHS 5U54GM104942-04NIH HHS CA192064NIH HHS CA194013
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a five-year survival rate of only 9%. PDAC is characterized by a dense, fibrotic stroma composed of extracellular matrix (ECM) proteins. This desmoplastic stroma is a hallmark of PDAC, representing a significant physical barrier that is immunosuppressive and obstructs penetration of cytotoxic chemotherapy agents into the tumor microenvironment (TME). Additionally, dense ECM promotes hypoxia, making tumor cells refractive to radiation therapy and alters their metabolism, thereby supporting proliferation and survival. In this review, we outline the significant contribution of fibrosis to the pathogenesis of pancreatic cancer, with a focus on the cross talk between immune cells and pancreatic stellate cells that contribute to ECM deposition. We emphasize the cellular mechanisms by which neutrophils and macrophages, specifically, modulate the ECM in favor of PDAC-progression. Furthermore, we investigate how activated stellate cells and ECM influence immune cells and promote immunosuppression in PDAC. Finally, we summarize therapeutic strategies that target the stroma and hinder immune cell promotion of fibrogenesis, which have unfortunately led to mixed results. An enhanced understanding of the complex interactions between the pancreatic tumor ECM and immune cells may uncover novel treatment strategies that are desperately needed for this devastating disease.

Indexed as

Immune ToleranceTumor MicroenvironmentCarcinoma, Pancreatic DuctalExtracellular MatrixHumansMacrophagesNeutrophilsPancreatic NeoplasmsPancreatic Stellate Cellsextracellular matrixfibrosisimmune cell modulationmacrophagesneutrophil extracellular trapneutrophilspancreatic ductal adenocarcinoma

Identifiers

PMID34204306
PMCPMC8234537
OpenAlexW3166338252

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.