ArticleScientific reports2019
Identification of a novel oncogenic mutation of FGFR4 in gastric cancer.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Article
- Malignant solitary fibrous tumor in the central nervous system treated with surgery, radiotherapy and anlotinib: A case report.World journal of clinical cases · 2022Article
- Identification of a novelFrontiers in oncology · 2022Article
- Comprehensive analysis of the prognostic value and immune infiltration ofFrontiers in oncology · 2022Article
- Review
- Novel Regulatory Factors and Small-Molecule Inhibitors of FGFR4 in Cancer.Frontiers in pharmacology · 2021Review
- FGFR Fusions in Cancer: From Diagnostic Approaches to Therapeutic Intervention.International journal of molecular sciences · 2020Review
- Downregulation of miR-484 is associated with poor prognosis and tumor progression of gastric cancer.Diagnostic pathology · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer remains one of the leading causes of cancer death worldwide. Despite intensive investigations of treatments over the past three decades, the poor prognosis of patients with unresectable advanced or recurrent gastric cancer has not significantly changed, and improved therapies are required. Here, we report the identification of an oncogenic mutation in FGFR4 in a human gastric tumour that leads to constitutive activation of its product, FGFR4. The G636C-FGFR4 tyrosine kinase domain mutation was found in 1 of 83 primary human gastric tumours. The G636C mutation increased FGFR4 autophosphorylation, and activated FGFR4 downstream signalling molecules and enhanced anchorage-independent cell growth when expressed in NIH/3T3 cells. 3D-structural analysis and modelling of FGFR4 suggest that G636C destabilizes an auto-inhibitory conformation and stabilizes an active conformation, leading to increased kinase activation. Ba/F3 cell lines expressing the G636C-FGFR4 mutant were significantly more sensitive to ASP5878, a selective FGFR inhibitor, than the control. Oral administration of ASP5878 significantly inhibited the growth of tumours in mice engrafted with G636C-FGFR4/3T3 cells. Together, our results demonstrate that mutationally activated FGFR4 acts as an oncoprotein. These findings support the therapeutic targeting of FGFR4 in gastric cancer.
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