Abstract:
:Telomerase regulation and telomere shortening act as a strong tumor suppressor mechanism in human somatic cells. Point mutations in the promoter of telomerase reverse transcriptase (TERT) are the most frequent non-coding mutation in cancer. These TERT promoter mutations (TPMs) create de novo ETS factor binding sites upstream of the start codon of the gene, which can be bound by different ETS factors. TPMs can occur early during tumorigenesis and are thought to be among the first mutations in melanoma, glioblastoma and hepatocellular carcinoma. Despite their association with increased TERT levels, TPMs do not prohibit telomere shortening and TPM-harboring cancers present with short telomeres. Their short telomere length combined with their high prevalence and specificity for cancer makes TPMs an attractive target for future therapeutic exploitation of telomerase inhibition and telomere deprotection-induced cell death.
journal_name
Curr Opin Genet Devjournal_title
Current opinion in genetics & developmentauthors
Lorbeer FK,Hockemeyer Ddoi
10.1016/j.gde.2020.02.001subject
Has Abstractpub_date
2020-02-01 00:00:00pages
56-62eissn
0959-437Xissn
1879-0380pii
S0959-437X(20)30004-6journal_volume
60pub_type
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journal_title:Current opinion in genetics & development
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journal_title:Current opinion in genetics & development
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journal_title:Current opinion in genetics & development
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journal_title:Current opinion in genetics & development
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journal_title:Current opinion in genetics & development
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journal_title:Current opinion in genetics & development
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