ArticleDigestive diseases and sciences2017
Mutation Detection of Fibroblast Growth Factor Receptor 3 for Infiltrative Hepatocellular Carcinoma by Whole-Exome Sequencing.
Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Comparing immunotherapy effectiveness for unresectable hepatocellular carcinoma: infiltrative versus non-infiltrative types in real-world settings.Therapeutic advances in medical oncology · 2025Article
- Review
- CSN1 facilitates proliferation and migration of hepatocellular carcinoma cells by upregulating cyclin A2 expression.Molecular medicine reports · 2021Article
- Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2020Article
- CSN5 Promotes Hepatocellular Carcinoma Progression by SCARA5 Inhibition Through Suppressing β-Catenin Ubiquitination.Digestive diseases and sciences · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGene data on infiltrative hepatocellular carcinoma (iHCC) are still unknown.
aimsThis study aims to identify the gene expression signature of iHCC compared with single nodular (SN)-type HCC according to the gross classification.
methodsThe whole-exome sequencing was performed in six matched HCC tumor/normal pairs (three infiltrative type and three single nodular type) from six patients who received curative hepatectomy. Subsequent validation using Sanger sequencing and real-time PCR was performed in 30 HCC tumor samples (15 infiltrative type and 15 single nodular type).
resultsFollowing whole-exome sequencing, Sanger sequencing, and bioinformatics analysis, it revealed significant difference of iHCC from SN-type HCC in gene patterns. Particularly, a typical growth factor receptor tyrosine kinase FGFR3 was predominantly mutated in iHCC. One nonsynonymous variant c.G285T (p.Q95H) and five additional mutations (c.G938A:p.G313D, c.G1291A:p.A431T, c.C1355G:p.T452R, c.C1377T:p.L459L, and c.A1445T:p.E482V) were investigated by whole-exome and Sanger sequencing, respectively. Immunohistochemical studies confirmed the specific expression of FGFR3 in iHCC samples.
conclusionOur studies indicated that FGFR3 may be a candidate oncogene in tumor progression and a promising therapeutic target in iHCC patients who had early recurrence.
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