ArticleNature communications2024
Mechanistic basis of atypical TERT promoter mutations.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Mechanistic and Clinical Perspectives on Traditional Chinese Medicine in Thyroid Cancer Management.Biomolecules & therapeutics · 2026Review
- Comprehensive molecular characterization of cutaneous squamous cell carcinoma reveals determinants of metastatic progression.medRxiv : the preprint server for health sciences · 2026Article
- Two-year dynamic risk stratification and adjuvant radioiodine efficacy in initial non-distant metastatic papillary thyroid carcinoma harboring TERT promoter mutations.Frontiers in oncology · 2026Article
- Review
- Advances in Computational Drug Repurposing, Driver Genes, and Therapeutics in Lung Adenocarcinoma.Biomolecules · 2025Review
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
- TERT-TP53 mutations: a novel biomarker pair for hepatocellular carcinoma recurrence and prognosis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Non-coding mutations in the TERT promoter (TERTp), typically at one of two bases -124 and -146 bp upstream of the start codon, are among the most prevalent driver mutations in human cancer. Several additional recurrent TERTp mutations have been reported but their functions and origins remain largely unexplained. Here, we show that atypical TERTp mutations arise secondary to canonical TERTp mutations in a two-step process. Canonical TERTp mutations create de novo binding sites for ETS family transcription factors that induce favourable conditions for DNA damage formation by UV light, thus creating a hotspot effect but only after a first mutational hit. In agreement, atypical TERTp mutations co-occur with canonical driver mutations in large cancer cohorts and arise subclonally specifically on the TERTp driver mutant chromosome homolog of melanoma cells treated with UV light in vitro. Our study gives an in-depth view of TERTp mutations in cancer and provides a mechanistic explanation for atypical TERTp mutations.
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Registered trials
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