Evidence map›Paper›PMID 41402556›Full record

ArticleBritish journal of cancer2026

Transgelin defines pro-tumorigenic cancer-associated fibroblasts in pancreatic cancer.

Xingxing Wang, Keiko Shinjo, Kohei Kumegawa, Reo Maruyama, Shinji Mii, Yukihiro Shiraki, Tastunori Nishimura, Yoshiteru Murofushi, Miho Suzuki, Takanobu Kabasawa and 5 more

Abstract read
In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Unravelling the pathogenesis and therapeutic approaches of pancreatic ductal adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  5. Article
  6. 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

15 authors.

Xingxing WangDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keiko ShinjoDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan. kshinjo@med.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0002-7797-6453
Kohei KumegawaCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID http://orcid.org/0000-0003-3732-2874
Reo MaruyamaCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID http://orcid.org/0000-0001-7166-5964
Shinji MiiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID http://orcid.org/0000-0001-8266-3235
Yukihiro ShirakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID http://orcid.org/0000-0003-3666-0556
Tastunori NishimuraDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yoshiteru MurofushiDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Miho SuzukiDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takanobu KabasawaDepartment of Pathology, Yamagata University, Yamagata, Japan.
Mitsuru FutakuchiDepartment of Pathology, Yamagata University, Yamagata, Japan.
Akinori KanaiLife Science Data Research Center, Graduate School of Frontier Sciences, the University of Tokyo, Chiba, Japan.
Yutaka SuzukiLife Science Data Research Center, Graduate School of Frontier Sciences, the University of Tokyo, Chiba, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yutaka KondoDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan. ykondo@med.nagoya-u.ac.jp.

Funding

Japan Agency for Medical Research and Development (AMED) P-CREATEJapan Agency for Medical Research and Development (AMED) SICORPMEXT | Japan Society for the Promotion of Science (JSPS) 23K06633
6 · The paper itself

Abstract

introductionPancreatic ductal adenocarcinoma (PDAC) is characterised by a pronounced desmoplastic reaction, predominantly composed of cancer-associated fibroblasts (CAFs), including myofibroblastic CAFs (myCAFs).

methodsWe performed a single-cell assay for transposase-accessible chromatin with high-throughput sequencing (scATAC-seq) and single-cell RNA sequencing (scRNA-seq) on pancreas tissues from KPC mice (LSL-Kras

resultsEpigenetic profiling uncovered heterogeneity within the myCAF population, revealing distinct subclusters characterised by specific transcription factor (TF) motifs, such as Srf, Cebpb, Prrx1, and Smad4. We identified three transcriptionally distinct myCAF subtypes, each enriched for unique TF-associated signalling pathways. Among the identified myCAF subtypes, Tagln emerged as a potential functional driver. Tagln knockout mice exhibited significantly reduced PDAC tumour burden compared to wild-type. Analysis of TCGA revealed that high TAGLN expression in PDAC samples was associated with poor survival.

conclusionsOur findings highlight the functional heterogeneity of myCAFs and identify TAGLN-expressing myCAFs as critical mediators of tumour progression, providing evidence that targeting stromal TAGLN may represent a promising therapeutic strategy for PDAC.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalMicrofilament ProteinsMuscle ProteinsPancreatic NeoplasmsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMice, KnockoutMicrofilament ProteinsMuscle Proteinstransgelin

Identifiers

PMID41402556
PMCPMC12858813

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.