ArticleOncogene2022
Loss of FGFR4 promotes the malignant phenotype of PDAC.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Dual Targeting of FGFR4 and PI3K-mTOR Suppresses Tumor-Associated Phenotypes in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Fgfr4 combined with inflammatory cytokines improves recurrence risk prediction in differentiated thyroid carcinoma: A retrospective cohort study.Journal of medical biochemistry · 2026Article
- High FGFR4 protein expression, but not FGFR1 or FGFR2, predicts poor prognosis in pancreatic ductal adenocarcinoma.BMC cancer · 2025Article
- Development of an in vitro method to assess the immunogenicity of biologics in the prevention of infectious diseases.Immunologic research · 2025Article
- Targeting FGFR4 abrogates HNF1A-driven metastasis in pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Differential activity of MAPK signalling defines fibroblast subtypes in pancreatic cancer.Nature communications · 2024Article
- Article
- FGF receptors mediate cellular senescence in the cystic fibrosis airway epithelium.JCI insight · 2024Article
- Association of the rs1966265 and rs351855Biomedicines · 2024Article
- TRPA1 Contributes to FGFR2c Signaling and to Its Oncogenic Outcomes in Pancreatic Ductal Adenocarcinoma-Derived Cell Lines.Cancers · 2024Article
Corrections and comments
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Authors and funding
26 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptomic analyses of pancreatic ductal adenocarcinoma (PDAC) have identified two major epithelial subtypes with distinct biology and clinical behaviours. Here, we aimed to clarify the role of FGFR1 and FGFR4 in the definition of aggressive PDAC phenotypes. We found that the expression of FGFR4 is exclusively detected in epithelial cells, significantly elevated in the classical PDAC subtype, and associates with better outcomes. In highly aggressive basal-like/squamous PDAC, reduced FGFR4 expression aligns with hypermethylation of the gene and lower levels of histone marks associated with active transcription in its regulatory regions. Conversely, FGFR1 has more promiscuous expression in both normal and malignant pancreatic tissues and is strongly associated with the EMT phenotype but not with the basal-like cell lineage. Regardless of the genetic background, the increased proliferation of FGFR4-depleted PDAC cells correlates with hyperactivation of the mTORC1 pathway both in vitro and in vivo. Downregulation of FGFR4 in classical cell lines invariably leads to the enrichment of basal-like/squamous gene programs and is associated with either partial or full switch of phenotype. In sum, we show that endogenous levels of FGFR4 limit the malignant phenotype of PDAC cells. Finally, we propose FGFR4 as a valuable marker for the stratification of PDAC patients.
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