Although arsenic is effective in the treatment of acute promyelocytic leukemia it also has carcinogenic side effects, but the exact carcinogenic mechanisms remain unclear. In 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.

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