Evidence map›Paper›PMID 26973408›Full record

ReviewWorld journal of gastroenterology2016

Key players in pancreatic cancer-stroma interaction: Cancer-associated fibroblasts, endothelial and inflammatory cells.

Michael Friberg Bruun Nielsen, Michael Bau Mortensen, Sönke Detlefsen

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
14.7field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 211 citations in OpenAlex.

  1. Prognostic biomarkers related to tumoral microenvironment in pancreatic ductal adenocarcinoma: a systematic review.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Ena/VASP-EVH1 inhibition prevents chemotaxis and metastasis by blocking the EVH1-WAVE2 interaction.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Nuclear Galectin-1 promotesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024
    Article
  19. Review
  20. Article

64 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Michael Friberg Bruun NielsenMichael Friberg Bruun Nielsen, Sönke Detlefsen, Department of Pathology, Odense University Hospital, University of Southern Denmark, 5000 Odense, Denmark.
Michael Bau MortensenMichael Friberg Bruun Nielsen, Sönke Detlefsen, Department of Pathology, Odense University Hospital, University of Southern Denmark, 5000 Odense, Denmark.
Sönke DetlefsenMichael Friberg Bruun Nielsen, Sönke Detlefsen, Department of Pathology, Odense University Hospital, University of Southern Denmark, 5000 Odense, Denmark.
Odense University Hospital · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PC) is the most aggressive type of common cancers, and in 2014, nearly 40000 patients died from the disease in the United States. Pancreatic ductal adenocarcinoma, which accounts for the majority of PC cases, is characterized by an intense stromal desmoplastic reaction surrounding the cancer cells. Cancer-associated fibroblasts (CAFs) are the main effector cells in the desmoplastic reaction, and pancreatic stellate cells are the most important source of CAFs. However, other important components of the PC stroma are inflammatory cells and endothelial cells. The aim of this review is to describe the complex interplay between PC cells and the cellular and non-cellular components of the tumour stroma. Published data have indicated that the desmoplastic stroma protects PC cells against chemotherapy and radiation therapy and that it might promote the proliferation and migration of PC cells. However, in animal studies, experimental depletion of the desmoplastic stroma and CAFs has led to more aggressive cancers. Hence, the precise role of the tumour stroma in PC remains to be elucidated. However, it is likely that a context-dependent therapeutic modification, rather than pure depletion, of the PC stroma holds potential for the development of new treatment strategies for PC patients.

Indexed as

Cell CommunicationAnimalsAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, Pancreatic DuctalDisease ProgressionEndothelial CellsEpithelial-Mesenchymal TransitionExtracellular Matrix ProteinsFibroblastsHumansInflammationPancreatectomyPancreatic NeoplasmsSignal TransductionStromal CellsTreatment OutcomeExtracellular Matrix ProteinsCancer-associated fibroblastDesmoplastic stromaInflammatory cellsPancreatic cancerPancreatic stellate cell

Identifiers

PMID26973408
PMCPMC4777992
OpenAlexW2326081342

What OpenQuestion holds

Textmetadata
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.