Abstract
Telomere attrition limits the replicative potential of most somatic cells. In contrast, tumor cells acquire immortality by continuous telomere maintenance which is predominantly due to the transcriptional upregulation of the limiting component of telomerase, hTERT (human telomerase reverse transcriptase). Recent findings have provided mechanistic insight into how oncogenic activation as well as derepression, often due to the inactivation of tumor suppressors, stimulate the hTERT promoter. Knowledge gained from the study of hTERT transcriptional regulation may prove instrumental in the development of cancer therapies directed at the suppression of telomerase activity in tumor cells.