Evidence map›Paper›PMID 26330349›Full record

ArticleBMC gastroenterology2015

Fibroblast activation protein-α-expressing fibroblasts promote the progression of pancreatic ductal adenocarcinoma.

Tomoya Kawase, Yumiko Yasui, Sohji Nishina, Yuichi Hara, Izumi Yanatori, Yasuyuki Tomiyama, Yoshihiro Nakashima, Koji Yoshida, Fumio Kishi, Masafumi Nakamura and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
3.3field-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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. Article
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  7. Article
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  11. TSPAN4Frontiers in immunology · 2025
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  16. Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  17. Article
  18. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024
    Article
  19. Article
  20. Review

9 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

11 authors at 2 institutions in 1 country.

Tomoya KawaseDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. oneworld_traveller@yahoo.co.jp.
Yumiko YasuiDepartment of Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan. yumikoy@med.kawasaki-m.ac.jp.
Sohji NishinaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. 018ep@med.kawasaki-m.ac.jp.
Yuichi HaraDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. yuich_h777@med.kawasaki-m.ac.jp.
Izumi YanatoriDepartment of Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan. yanatori@med.kawasaki-m.ac.jp.
Yasuyuki TomiyamaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. tomiyama@med.kawasaki-m.ac.jp.
Yoshihiro NakashimaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. makazi777@med.kawasaki-m.ac.jp.
Koji YoshidaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. kojiyos@med.kawasaki-m.ac.jp.
Fumio KishiDepartment of Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan. kishi@med.kawasaki-m.ac.jp.
Masafumi NakamuraDepartment of Digestive Surgery, Kawasaki Medical School, Kurashiki, Japan. mnaka@surg1.med.kyushu-u.ac.jp.
Keisuke HinoDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan. khino@med.kawasaki-m.ac.jp.
Kawasaki Medical School · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive desmoplastic stromal response. Fibroblast activation protein-α (FAP) is best known for its presence in stromal cancer-associated fibroblasts (CAFs). Our aim was to assess whether FAP expression was associated with the prognosis of patients with PDAC and to investigate how FAP expressing CAFs contribute to the progression of PDAC.

methodsFAP expression was immunohistochemically assessed in 48 PDAC specimens. We also generated a fibroblastic cell line stably expressing FAP, and examined the effect of FAP-expressing fibroblasts on invasiveness and the cell cycle in MiaPaCa-2 cells (a pancreatic cancer cell line).

resultsStromal FAP expression was detected in 98% (47/48) of the specimens of PDAC, with the intensity being weak in 16, moderate in 19, and strong in 12 specimens, but was not detected in the 3 control noncancerous pancreatic specimens. Patients with moderate or strong FAP expression had significantly lower cumulative survival rates than those with negative or weak FAP expression (mean survival time; 352 vs. 497 days, P = 0.006). Multivariate analysis identified moderate to strong expression of FAP as one of the factors associated with the prognosis in patients with PDAC. The intensity of stromal FAP expression was also positively correlated to the histological differentiation of PDAC (P < 0.05). FAP-expressing fibroblasts promoted the invasiveness of MiaPaCa-2 cells more intensively than fibroblasts not expressing FAP. Coculture with FAP-expressing fibroblasts significantly activated cell cycle shift in MiaPaCa-2 cells compared to coculture with fibroblasts not expressing FAP. Furthermore, coculture with FAP expressing fibroblasts inactivated retinoblastoma (Rb) protein, an inhibitor of cell cycle progression, in MiaPaCa-2 cells by promoting phosphorylation of Rb.

conclusionsThe present in vitro results and the association of FAP expression with clinical outcomes provide us with a better understanding of the effect of FAP-expressing CAFs on the progression of PDAC.

Indexed as

AgedCarcinoma, Pancreatic DuctalCell Cycle CheckpointsCell Line, TumorCoculture TechniquesDisease ProgressionEndopeptidasesFemaleFibroblast Activation Protein AlphaFibroblastsGelatinasesHumansMaleMembrane ProteinsMiddle AgedNeoplasm InvasivenessEndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsRetinoblastoma ProteinSerine Endopeptidases

Identifiers

PMID26330349
PMCPMC4556412
OpenAlexW1805321156

What OpenQuestion holds

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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.