ArticleVirchows Archiv : an international journal of pathology2014
Frequency of TERT promoter mutations in primary tumors of the liver.
Article in Virchows Archiv : an international journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 67 citations in OpenAlex.
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- Beyond histology: A tissue algorithm predictive of post-surgical recurrence in hepatocellular carcinomas, including TERT promoter mutation.Virchows Archiv : an international journal of pathology · 2025Article
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- GABP couples oncogene signaling to telomere regulation in TERT promoter mutant cancer.Cell reports · 2022Article
- Correlation of molecular alterations with pathological features in hepatocellular carcinoma: Literature review and experience of an Italian center.World journal of gastroenterology · 2022Review
- De novo identification of maximally deregulated subnetworks based on multi-omics data with DeRegNet.BMC bioinformatics · 2022Article
- Human MettL3-MettL14 RNA adenine methyltransferase complex is active on double-stranded DNA containing lesions.Nucleic acids research · 2021Article
- Hepatocellular adenoma in men: A nationwide assessment of pathology and correlation with clinical course.Liver international : official journal of the International Association for the Study of the Liver · 2021Article
- TERT promoter mutation in sebaceous neoplasms.Virchows Archiv : an international journal of pathology · 2021Article
- Exploring the Interplay of Telomerase Reverse Transcriptase and β-Catenin in Hepatocellular Carcinoma.Cancers · 2021Review
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- Gene networks and transcriptional regulators associated with liver cancer development and progression.BMC medical genomics · 2021Article
- Identification of Potential Biomarkers for Liver Cancer Through Gene Mutation and Clinical Characteristics.Frontiers in oncology · 2021Article
- Review
- Frequency of somatic mutations inOncology letters · 2020Article
- The role of telomeres and telomerase in cirrhosis and liver cancer.Nature reviews. Gastroenterology & hepatology · 2019Review
- Structural basis for reactivating the mutant TERT promoter by cooperative binding of p52 and ETS1.Nature communications · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional regulation of the TERT gene is a major cause of the cancer-specific increase in telomerase activity. Recently, frequent somatic mutations in the TERT promoter have been described in several tumor entities such as melanoma, glioblastoma, bladder cancer, and hepatocellular carcinoma. By generating a putative consensus binding site for ETS transcription factors within the TERT promoter, these mutations are predicted to increase promoter activity and TERT transcription. In order to improve the understanding of the role of TERT promoter mutation in liver tumorigenesis, the mutational status of the TERT promoter was analyzed in 78 hepatocellular carcinomas, 15 hepatocellular adenomas, and 52 intrahepatic cholangiocarciomas. The promoter region of TERT was screened for the two hotspot mutations using PCR and restriction fragment length analysis, utilizing the introduction of novel restriction sites by the somatic mutations. TERT promoter mutation was found in 37 of 78 hepatocellular carcinomas (47 %) and was restricted to the -124C>T mutation. Frequency of mutations was associated with grade of differentiation ranging from 39 % in well-differentiated tumors to 73 % in high-grade hepatocellular carcinomas. TERT promoter mutations were not found in 15 hepatocellular adenomas and 52 intrahepatic cholangiocarcinomas. These data show that TERT promoter mutation is the most frequent genetic alteration in hepatocellular carcinoma known at this time. The striking predominance of the -124C>T mutation compared with other tumor entities suggest a biological difference of the two hotspot mutations. Analysis of TERT promoter mutation might become a diagnostic tool distinguishing hepatocellular adenoma from well-differentiated hepatocellular carcinoma.
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