Evidence map›Paper›PMID 28978805›Full record

ArticleJCI insight2017

Fibroblast activation protein augments progression and metastasis of pancreatic ductal adenocarcinoma.

Albert Lo, Chung-Pin Li, Elizabeth L Buza, Rachel Blomberg, Priya Govindaraju, Diana Avery, James Monslow, Michael Hsiao, Ellen Puré

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 156 citations in OpenAlex.

  1. Article
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  12. Article
  13. The fibroinflammatory response in cancer.Nature reviews. Cancer · 2025
    Review
  14. HMGA2 Expression Predicts Subtype, Survival, and Treatment Outcome in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Panoramic tumor microenvironment in pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review

31 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

9 authors at 3 institutions in 2 countries.

Albert LoDepartment of Biomedical Sciences and.
Chung-Pin LiDivision of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Elizabeth L BuzaDepartment of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Rachel BlombergDepartment of Biomedical Sciences and.
Priya GovindarajuDepartment of Biomedical Sciences and.
Diana AveryDepartment of Biomedical Sciences and.
James MonslowDepartment of Biomedical Sciences and.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Ellen PuréDepartment of Biomedical Sciences and.
University of Pennsylvania · USGenomics Research Center, Academia Sinica · TWNational Yang Ming Chiao Tung University · TW

Funding

Use of Genetically Engineered T cells Targeting Tumor Stroma to Treat Lung CancerR01CA172921 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ALBELDA, STEVEN MARK · 2013 to 2017
$1.8M
Fibroblast Activation Protein in the Tumor Microenvironment in Lung CancerR01CA141144 · NCI · WISTAR INSTITUTE · PI PURE', ELLEN · 2010 to 2014
$1.6M
The role of the stromal cell surface protease FAP in pancreatic cancerR21CA169741 · NCI · WISTAR INSTITUTE · PI PURE', ELLEN · 2013 to 2014
$383k
NCI NIH HHS R01 CA141144NCI NIH HHS R01 CA172921NCI NIH HHS R21 CA169741
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinomas (PDAs) are desmoplastic and can undergo epithelial-to-mesenchymal transition to confer metastasis and chemoresistance. Studies have demonstrated that phenotypically and functionally distinct stromal cell populations exist in PDAs. Fibroblast activation protein-expressing (FAP-expressing) cells act to enhance PDA progression, while α-smooth muscle actin myofibroblasts can restrain PDA. Thus, identification of precise molecular targets that mediate the protumorigenic activity of FAP+ cells will guide development of therapy for PDA. Herein, we demonstrate that FAP overexpression in the tumor microenvironment correlates with poor overall and disease-free survival of PDA patients. Genetic deletion of FAP delayed onset of primary tumor and prolonged survival of mice in the KPC mouse model of PDA. While genetic deletion of FAP did not affect primary tumor weight in advanced disease, FAP deficiency increased tumor necrosis and impeded metastasis to multiple organs. Lineage-tracing studies unexpectedly showed that FAP is not only expressed by stromal cells, but can also be detected in a subset of CD90+ mesenchymal PDA cells, representing up to 20% of total intratumoral FAP+ cells. These data suggest that FAP may regulate PDA progression and metastasis in cell-autonomous and/or non-cell-autonomous fashions. Together, these data support pursuing FAP as a therapeutic target in PDA.

Indexed as

AdultAgedAged, 80 and overAnimalsBiomarkers, TumorCarcinoma, Pancreatic DuctalDisease ProgressionEndopeptidasesFemaleFibroblast Activation Protein AlphaGelatinasesHeterograftsHumansKaplan-Meier EstimateMaleMembrane ProteinsBiomarkers, TumorEndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsSerine Endopeptidases

Identifiers

PMID28978805
PMCPMC5841864
OpenAlexW2761578140

What Socratic 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 Socratic graph.