Unlimited replicative potential and widespread genomic disarray are among the most common characteristics exhibited by human cancer cells. Although several distinct molecular pathways regulate specific aspects of each of these phenotypes, specialized chro ...mosomal terminal structures, termed telomeres act as essential regulators of both cell life span and chromosomal integrity. Telomeres are dynamic DNA-protein complexes that cap the ends of linear chromosomes, preventing detrimental chromosome rearrangements and defending against genomic instability and the associated risk of cancer. Telomeres shorten every time a cell divides because of incomplete DNA replication and DNA end processing. When telomere length reaches a critical point, cells stop dividing and undergo replicative senescence. Mammalian telomeres are composed of tandem repeats of the TTAGGG sequence and an array of associated proteins. Loss of telomeric capping leads to chromosome end-to-end fusion and triggers cell cycle arrest and apoptosis that contribute to the aging process. When they are not being replicated telomeres are bound by a protein or protein complex whose function is to protect the telomere from degradation. Telomerase, also called telomere terminal transferase, prevents telomere shortening by using its integral RNA component as a template to add hexameric repeats TTAGGG sequences to the mammalian telomeres to compensate for the loss of base pairs that occurs after subsequent rounds of DNA replication. It is found in fetal tissues, adult germ cells, and tumor cells and has a very low, almost undetectable activity in somatic cells. Telomerase has two essential components, an RNA molecule called TERC (Telomerase RNA Component; hTERC in humans), and a catalytic subunit called TERT (Telomerase Reverse Transcriptase; hTERT in humans).
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