At the ends of chromosome are special pieces of DNA called telomeres. Think of it as the little tip that caps off a shoelace. The telomeres send signals to the cells to let them know it’s the end point, not a break that should be repaired.
Over time, as cells reproduce, the telomeres become shorter and eventually no longer do their job. The cells then have a higher risk of mutating into cancer.
But, a new study finds, if the telomere becomes dysfunctional at any point – regardless of shortening – it can trigger a cancer event. The study, by researchers at the University of Michigan Comprehensive Cancer Center, was done in mice generally prone to develop cancer. The mice that also had dysfunctional telomeres were particularly prone to develop the usually ultra-rare adrenocortical cancer. This is the first mouse model to specifically address this rare but lethal type of cancer.
“Usually when telomeres get short, they also seem to get deprotected. No one’s been able to say if it’s the shortening or the deprotection that causes cancer to arise. In this study, we were able to show that deprotection alone, even in the absence of a short telomere, is enough to trigger cancer.