Alternative lengthening of telomeres, telomerase, and cancer

Abstract 

Telomere length may be maintained in cancer cells by telomerase or an alternative lengthening of telomeres (ALT) mechanism. Low levels of telomerase activity have been detected in some normal somatic cells and presumably some types of normal cells also have low levels of an ALT-like activity. It is hypothesized here that inherited abnormalities of these and other aspects of telomere maintenance may contribute to cancer and ageing. The telomere length maintenance mechanisms are similar in that activation of each is associated with immortalization. They may also confer other properties on cancer cells, however, and the nature of these additional properties may be different for telomerase and ALT. It is expected that these similarities and differences will have implications for prognosis and treatment.

Telomerase, hTERT, Cancer, Alternative lengthening of telomeres, Senescence, Immortalization, Cancer, Ageing, Down syndrome, Werner syndrome, Ataxia telangiectasia, Dyskeratosis congenita