CancerQuest | Oncogenes: Telomerase

Due to the nature of the DNA replication process the ends (telomeres) of our chromosomes become shortened during each cell division. The shortening of the chromosomes serves to limit the number of times any given cell can undergo division. When telomeres shorten to a critical length the cell is unable to replicate its DNA without losing vital genetic material. At this point normal cells enter cellular senescence, or growth arrest, after which no further cell division takes place.

Cancer cells have the ability to replicate without reaching a state of senescence. In many cancers the ability to divide without limit is achieved by the production of an enzyme called telomerase. Telomerase maintains the ends of chromosomes so that they do not shorten. Telomerase is a normal protein that is present in cells during fetal development. In most cells of an adult human, telomerase is not present as the gene for the enzyme is not being expressed (transcribed and translated). However, in some cancer cells the necessary task of achieving unlimited replication is made possible by the reactivation of the gene that codes for telomerase.

The animation on the right below depicts the lengths of chromosomes both with (right) and without (left) active telomerase.

In cancer cells that do not possess telomerase activity, shortening of chromosomes is thought to be prevented by other mechanisms. The maintenance of telomere length allows for unlimited cell division. The gene that codes for the active component of the telomerase enzyme, hTERT, is considered a proto-oncogene because abnormal expression contributes to unregulated cell growth.