ArticleJournal of gastroenterology2026
YAP1-driven tumor-like cancer-associated fibroblasts modulate biomechanics of pancreatic ductal adenocarcinoma.
Article in Journal of gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
Who cites it
3 citing papers in PubMed.
- The tumor microenvironment in pancreatic cancer: from composition to therapeutic targeting.Biochemical Society transactions · 2026Review
- Review
- The mechano-immunological landscape in the tumor microenvironment: From mechanical sensing to a new therapeutic paradigm.Materials today. Bio · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundIn pancreatic ductal adenocarcinoma (PDAC), activation of Yes-associated protein 1 (YAP1) is linked to increased extracellular matrix (ECM) stiffness, yet how YAP1 interacts with cancer-associated fibroblasts (CAFs) and their subtypes to promote stromal remodeling remains unclear.
methodsUtilizing single-cell RNA sequencing (scRNA-seq) data to identify CAF subsets; validating the role of a specific subset, tumor-like CAFs (tCAFs), in YAP1-dependent promotion of ECM stiffness, epithelial-mesenchymal transition (EMT) combining the YAP1 inhibitor verteporfin with gemcitabine in KPC mouse models to assess effects on tCAF function, stromal stiffness, and survival; and employing magnetic resonance elastography (MRE) to quantify tumor stiffness in PDAC patients and mouse models.
resultsscRNA-seq identified a novel CAF subset (tCAFs) enriched in tumors with high YAP1 activity; tCAFs and mCAFs can mutually differentiate, and this process is regulated by YAP1 activity; in KPC mice, the combination of verteporfin and gemcitabine suppressed tCAF function, reduced stromal stiffness, and improved survival; MRE can accurately quantify tumor stiffness in PDAC patients; elevated YAP1 activity induces a stiffer, more highly cross-linked ECM, which is associated with increased tumor aggressiveness and shortened survival.
conclusionsYAP1 and tumor-like CAFs (tCAFs) play a pivotal role in driving desmoplasia in PDAC. YAP1 mediates the conversion of mCAFs to tCAFs and remodels the extracellular matrix (ECM), while high YAP1 activity in tCAFs regulates EMT induction to propel disease progression. Targeting the YAP1-tCAF axis can suppress desmoplasia and improve therapeutic outcomes. Magnetic resonance elastography (MRE) holds significant potential for non-invasive monitoring of stromal mechanics, offering a new perspective for stromal therapies in PDAC.
Indexed as
Identifiers
41634388What Socratic holds
Registered trials
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.