Evidence map›Paper›PMID 40303408›Full record

ArticleFrontiers in immunology2025

Heterogenous cancer-associated fibroblasts related tumor microenvironment marked by CD10/KLF4/TIAM1 were identified in pancreatic adenocarcinoma by integrated transcriptomics.

Yu Wan, Qiong Hu, Kai Sun, Jing Shi, Limei Liu, Xiangsong Zhang, Jianjun Huang, Chulan Gong, Jinting Liu, Haijiu Wang and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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.

Yu Wan *Department of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.
Qiong Hu *Department of Cadre Medical, Guizhou Provincial People's Hospital, Guiyang, China.
Kai SunSchool of Biomedical Engineering, Tsinghua University, Beijing, China.
Jing ShiDepartment of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.
Limei LiuDepartment of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.
Xiangsong ZhangDepartment of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.
Jianjun HuangDepartment of Breast Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Chulan GongDepartment of Breast Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Jinting LiuDepartment of Breast Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Haijiu WangDepartment of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.
Jun YanDepartment of Hepatobiliary and Pancreatic Surgery, Qinghai University Affiliated Hospital, Xining, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by a dense and heterogeneous tumor microenvironment (TME) composed of various cancer-associated fibroblasts (CAFs). In this study, we explored the composition and proportions of CAF subtypes within the PDAC TME and identified three distinct CAF-related TME subtypes: iCAF-rich, myCAF-rich, and PSC-rich. We observed significant heterogeneity in CAF populations across different patients, which correlated with patient prognosis and the mechanical and fibrotic properties of the TME. Our analysis revealed that these CAF subtypes exhibit distinct gene expression profiles, with the myCAF-rich subtype showing upregulation of hypoxia- and glycolysis-related genes, such as LDHA. Furthermore, gene set and survival analyses demonstrated that specific CAF subtypes harbor unique protective and risk factors, which were non-overlapping between the subtypes. These findings suggest that the heterogeneity of CAF subtypes plays a critical role in PDAC progression and therapeutic response. By utilizing multiplex immunohistochemistry and spatial transcriptomics, we also identified key CAF subpopulations, such as iCAF_17, iCAF_19, and myCAF_12, which were found to interact closely with tumor cells and macrophages. In chemotherapy-treated patients, myCAFs were positioned at the tumor boundary, potentially acting as a barrier to tumor invasion. This study provides novel insights into CAF-related TME subtypes, offering a foundation for future therapeutic strategies targeting CAFs in PDAC.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalKruppel-Like Transcription FactorsPancreatic NeoplasmsTranscriptomeTumor MicroenvironmentBiomarkers, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansKruppel-Like Factor 4MaleMiddle AgedPrognosisBiomarkers, TumorKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription Factorscancer-associated fibroblastspancreatic adenocarcinomaScRNA-seqspatial transcriptomicstumor microenvironment

Identifiers

PMID40303408
PMCPMC12038268

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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.