Evidence map›Paper›PMID 39585543›Full record

ReviewMedical oncology (Northwood, London, England)2024

Exploring the role of antigen-presenting cancer-associated fibroblasts and CD74 on the pancreatic ductal adenocarcinoma tumor microenvironment.

Michael E Thomas, Emily Jie, Austin M Kim, Trenton G Mayberry, Braydon C Cowan, Harrison D Luechtefeld, Mark R Wakefield, Yujiang Fang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Vorinostat Potentiates Chemoimmunotherapy in Immune-Enriched Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. POSTNOncology reports · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. 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

8 authors.

Michael E ThomasDepartment of Microbiology, Immunology and Pathology, Des Moines University College of Osteopathic Medicine, West Des Moines, IA, 50266, USA.
Emily JieDepartment of Psychology, Iowa State University, Ames, IA, 50011, USA.
Austin M KimDepartment of Microbiology, Immunology and Pathology, Des Moines University College of Osteopathic Medicine, West Des Moines, IA, 50266, USA.
Trenton G MayberryDepartment of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA.
Braydon C CowanDepartment of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA.
Harrison D LuechtefeldDepartment of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA.
Mark R WakefieldDepartment of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA.
Yujiang FangDepartment of Microbiology, Immunology and Pathology, Des Moines University College of Osteopathic Medicine, West Des Moines, IA, 50266, USA. yujiang.fang@dmu.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has proven to be a formidable cancer primarily due to its tumor microenvironment (TME). This highly desmoplastic, hypoxic, and pro-inflammatory environment has not only been shown to facilitate the growth and metastasis of PDAC but has also displayed powerful immunosuppressive capabilities. A critical cell involved in the development of the PDAC TME is the fibroblast, specifically the antigen-presenting cancer-associated fibroblast (apCAF). The pro-inflammatory environment of PDAC induces the proliferation of apCAFs, promoting immunosuppression through immune cell inactivation, immune response regulation, and expression of CD74. In conjunction with apCAFs and tumor cells, CD74 serves as a versatile promoter of PDAC by preventing tumor antigen-expression on tumor cells, upregulating the expression of immunosuppressive chemical mediators, and activating proliferative pathways to induce PDAC malignancy. This review will highlight critical mediators and pathways that promote the PDAC stroma and TME with its hypoxic and immunosuppressive properties. Further, we will highlight the nature of apCAFs and CD74, their specific roles in the PDAC TME, and their potential as targets for immunotherapy.

Indexed as

Antigens, Differentiation, B-LymphocyteCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsTumor MicroenvironmentAnimalsHistocompatibility Antigens Class IIHumansAntigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIinvariant chainAntigen-presenting cancer-associated fibroblastsCD74Pancreatic ductal adenocarcinomaPathogenesisTumor microenvironment

Identifiers

What OpenQuestion holds

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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.