Telomeres consistent of repetitive subunits of DNA at the ends of chromosomes, where they protect chromosomes from DNA damage. In aged humans, telomere shortening and DNA damage likely have occurred. Reintroducing telomerase activity in these individuals--where telomerase activity is low or absent in adults--may increase the risk of tumorigenesis by maintaining telomeres in cells with significant DNA damage, thereby avoiding DNA damage-induced cell death or senescence.
This may differ from the animal model, where the timeline for DNA damage exposure may be limited due to temporality of the model system studied. Therefore, the reintroduction of telomerase may not unveil additional risk of cancer.
Also, the activity of telomerase is being further investigated, as it has been shown to have other activities--e.g. in transactivation of gene expression--besides lengthening telomeres (Telomerase modulates Wnt signalling by association with target gene chromatin). These effects must be investigated when recapitulating telomerase activity in adults.