Evidence map›Paper›PMID 37190281›Full record

ReviewCancers2023

Overcoming the Fibrotic Fortress in Pancreatic Ductal Adenocarcinoma: Challenges and Opportunities.

Kay K Myo Min, Charlie B Ffrench, Claire F Jessup, Mia Shepherdson, Savio George Barreto, Claudine S Bonder

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mechanisms of Pericyte-Mediated Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. ZNF821 as a potential biomarker associated with immune infiltration in pancreatic adenocarcinoma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Article
  8. Exploring the interactions of integrins and CEACAM6 (Review).Experimental and therapeutic medicine · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Kay K Myo MinCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA 5000, Australia.
Charlie B FfrenchCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA 5000, Australia.ORCID 0000-0001-9069-3450
Claire F JessupCollege of Medicine & Public Health, Flinders University, Bedford Park, SA 5042, Australia.
Mia ShepherdsonCollege of Medicine & Public Health, Flinders University, Bedford Park, SA 5042, Australia.ORCID 0000-0002-6004-4764
Savio George BarretoCollege of Medicine & Public Health, Flinders University, Bedford Park, SA 5042, Australia.ORCID 0000-0002-4999-5657
Claudine S BonderCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA 5000, Australia.ORCID 0000-0001-9875-967X
Flinders University · AUSouth Australia Pathology · AU

Funding

National Health and Medical Research Council GNT2021009PanKind 21.R7.INV.CB.UOSA.6.2
6 · The paper itself

Abstract

An overabundance of desmoplasia in the tumour microenvironment (TME) is one of the defining features that influences pancreatic ductal adenocarcinoma (PDAC) development, progression, metastasis, and treatment resistance. Desmoplasia is characterised by the recruitment and activation of fibroblasts, heightened extracellular matrix deposition (ECM) and reduced blood supply, as well as increased inflammation through an influx of inflammatory cells and cytokines, creating an intrinsically immunosuppressive TME with low immunogenic potential. Herein, we review the development of PDAC, the drivers that initiate and/or sustain the progression of the disease and the complex and interwoven nature of the cellular and acellular components that come together to make PDAC one of the most aggressive and difficult to treat cancers. We review the challenges in delivering drugs into the fortress of PDAC tumours in concentrations that are therapeutic due to the presence of a highly fibrotic and immunosuppressive TME. Taken together, we present further support for continued/renewed efforts focusing on aspects of the extremely dense and complex TME of PDAC to improve the efficacy of therapy for better patient outcomes.

Indexed as

desmoplasiaimmunotherapypancreatic ductal adenocarcinomatargeted therapytumour microenvironment

Identifiers

PMID37190281
PMCPMC10137060
OpenAlexW4366281330

What Socratic 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 Socratic graph.