I'll make the same comment on this as before, which is that the lack of cancer is the interesting outcome, and that there isn't yet a robust defensible accounting of exactly why telomerase is extending life in these mice. For example, effects on mitochondrial function that lower their damage rate over time have been proposed as another activity for telomerase. It isn't beyond the pale to think it as important as increased stem cell activity.

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Telomeres are caps of repeated DNA sequences at the end of chromosomes. A little telomere length is lost every time a cell divides and its DNA is replicated, and this is one portion of the limiting mechanism that causes the somatic cells that make up the overwhelming majority of tissues to divide only a set number of times and then destroy themselves. Stem cells on the other hand make use of the enzyme telomerase to add repeated DNA sections to the ends of their telomeres as needed. They must maintain lengthy telomeres as it is their job is to continually spin off new long-telomere somatic cells to keep tissues running smoothly. This is a considerable simplification of the actual situation, but it is good enough for this discussion. The important point here is that if you measure average telomere length in a given tissue, and immune cells from blood are the most commonly used for this purpose at the moment, what you are in fact measuring is a some combination of present cell replication rates, cell replenishment rates, and telomerase activity.

There is a statistically significant correlation between average telomere lengths in immune cells and age and illness across a population. This isn't so useful for any given individual looking at a number and trying to figure out whether or not it means anything for future health, but it is true that the older and more ill a person is, the more likely it is for average telomere length in immune cells to be comparatively short. Is this meaningful to efforts to extend life? That is a question worth asking twice, given that telomere length measures look very much like a secondary marker resulting from the characteristic decline of stem cell activity and tissue maintenance with advancing age, and we really want to aim at primary causes rather then secondary and later mechanisms.

Nonetheless, a fair number of researchers are interested in trying to lengthen telomeres as a potential way to treat illness or lengthen life, and in recent years one research group has used gene therapy to raise levels of telomerase in mice. This turns out to extend mouse life span, with the caveats that (a) short-lived mammals like mice actually have quite different telomere dynamics from long-lived mammals such as we humans, so it is far from clear as to what the same thing would do in people, and (b) it is by no means certain what exactly is going on under the hood here. Is telomerase keeping somatic cells alive for longer, it is increasing stem cell activity, is it perhaps interacting with mitochondria in some way to reduce their contribution to aging, or is some other as yet undiscovered mechanism is at work?

Researchers will come to a conclusion at some point, as there seems to be slow but steady progress towards further investigations of telomerase gene therapy in mice. The same group that pioneered this approach is now heading down the traditional path of attempts to apply this treatment as a late stage intervention for age-related disease and dysfunction. They do this because it is still the only practical way to bring treatments to the clinic these days: approaches are inevitably sidelined into marginal applications intended to be applied after the damage is done. It is a ridiculous situation, and one that causes immense damage to the pace of progress by diverting researchers away from producing methods of prevention.