Abstract
Telomere shortening at the ends of chromosomes is considered as one of the mechanisms for tumor prevention since critically shortened telomeres elicit a DNA damage response and induce cellular senescence. Immortality of cancer cells depends on telomere maintenance by telomerase. Thus, telomerase inhibitors have a potential to be new anticancer molecular targeting agents. Tankyrase 1, which enhances telomere access to telomerase, is another target for telomere-directed cancer therapeutics. It has been long postulated that anticancer effects of telomerase inhibitors depend on telomere shortening. Recently, however, new reports suggest another working mechanism for the agents, which is independent of telomere status of the target cancer cells.
