More insight into the mechanism behind telomere maintenance and replication shed light on its role in cancer as well as aging. It was discovered that in 80-90% of cancers, an increase in telomerase activity can be shown. This indicates the role telomere shortening may play in preventing unwanted mutations and cancer. Once cells divide a certain number of times in healthy cells, unprotected and shortened telomeres trigger senescence and apoptosis. With overactive telomerase, this shortening is prevented and cells would be able to proliferate uncontrollable and an unlimited number of times. This mechanism of induced senescence and apoptosis in cells with improper telomere function appears to be regulated by the tumor suppressor gene p53, which acts by binding damaged DNA and promotes p21 activity, a CDK inhibitor which induces cell arrest pathways. Since p53 function is inhibited in 70-80% of cancers, this provides a major hurdle for biologists moving forward in targeting drug therapies towards cancer cells with impaired telomeres.
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