Arsenic and old telomerase
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Correspondence: Tudor Toma t.toma@ic.ac.uk
Genome Biology 2001, 2:spotlight-20011127-01 doi:10.1186/gb-spotlight-20011127-01
The electronic version of this article is the complete one and can be found online at:
| Published: | 27 November 2001 |
© 2001 BioMed Central Ltd
Research news
Although arsenic is effective in the treatment of acute promyelocytic leukaemia, it also has carcinogenic side effects, but the exact mode of action in carcinogenesis remains unclear. In the November Journal of Clinical Investigation, Wen-Chien Chou and colleagues from Johns Hopkins University School of Medicine, Baltimore, US show that, at clinically relevant doses, arsenic inhibits the transcription of the reverse-transcriptase subunit of the human telomerase gene (hTERT).
Chou et al. found that exposing NB4 leukemia cells to arsenic inhibited transcription of the hTERT gene by decreasing c-Myc and Sp1 transcription factor activities. Decreased hTERT activity led to chromosomal end lesions, which promoted either genomic instability and carcinogenesis or cancer cell death (J Clin Invest 2001, 108:1541-1547).
"These results may explain the seemingly paradoxical carcinogenic and antitumor effects of arsenic", concluded Chou.
References
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Chou W-C, Hawkins AL, Barrett JF, Griffin CA, Dang CV: Arsenic inhibition of telomerase transcription leads to genetic instability. J Clin Invest 2001, 108:1541-1547.
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