The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Cancer-associated TERT promoter mutations abrogate telomerase silencing
Open accessAbstract
Mutations in the human telomerase reverse transcriptase (TERT) promoter are the most frequent non-coding mutations in cancer, but their molecular mechanism in tumorigenesis has not been established. We used genome editing of human pluripotent stem cells with physiological telomerase expression to elucidate the mechanism by which these mutations contribute to human disease. Surprisingly, telomerase-expressing embryonic stem cells engineered to carry any of the three most frequent TERT promoter mutations showed only a modest increase in TERT transcription with no impact on telomerase activity. However, upon differentiation into somatic cells, which normally silence telomerase, cells with TERT promoter mutations failed to silence TERT expression, resulting in increased telomerase activity and aberrantly long telomeres. Thus, TERT promoter mutations are sufficient to overcome the proliferative barrier imposed by telomere shortening without additional tumor-selected mutations. These data establish that TERT promoter mutations can promote immortalization and tumorigenesis of incipient cancer cells.
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Cites
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BackgroundMethodExtension of Life-Span by Introduction of Telomerase into Normal Human Cells
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The transcription factor GABP selectively binds and activates the mutant TERT promoter in cancer
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Cited by
Telomeres in cancer: tumour suppression and genome instability
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Roles of telomeres and telomerase in cancer, and advances in telomerase-targeted therapies
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Role of Telomeres and Telomerase in Aging and Cancer
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Common genetic variation drives molecular heterogeneity in human iPSCs
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Induced Pluripotent Stem Cells Meet Genome Editing
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“Facing this challenge, recent studies used creative ways to take advantage of NHEJmeditated genome editing and the fact that the simultaneous expression of two nucleases can meditate the excision or inversion of the sequence internal to the two SSN (Chiba et al., 2015; (Chen et al., 2011; Young et al., 2016).”
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Metadata
- Authors
- Chiba, K., Johnson, J. Z., Vogan, J. M., Wagner, T., Boyle, J. M., & Hockemeyer, D.
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2015-07-21
- Volume
- 4
- ISSN
- 2050-084X (ISSN-L)
- OpenAlex
- W2160562062
- Cited by
- 251
- References
- 17
- FWCI
- 20.88
- Type
- journal article
- Language
- en
- Open access
- gold
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