Biochemistry is a resource-intensive science - the closer you look, the more detail there is to find. At our present level of understanding, everything is open to closer inspection - biotechnology and medical research could make good use of far more resources than are presently devoted to progress.
Everything is more complex than you think, and more complex than we'd like for rapid progress. Take telomeres, for example: much as we'd like their relationship to aging and cancer to be comparatively straightforward, there is a great deal of complexity going on in there. Telomere length is one part of a dynamic, evolved system churning away in all our bodies - the grand balance between maintaining the ability to heal damage and maintaining the ability to suppress cancer as we age. Take a look at these examples:
Telomeres control cell division in the body - by gradually becoming shorter they can tell cells when it is time to stop dividing. However when telomeres stop working properly, they can cause the cells to mutate and start dividing uncontrollably, which can lead to the formation of tumours.
The Cardiff study used ground-breaking techniques to study telomeres in human cells. The researchers found the critical length at which telomeres stop working and also that some telomeres can be shortened or deleted at random, without any external cause.
This study threw up a number of significant results. The fact that telomeres can be deleted at random in otherwise normal cells indicates that some of the earliest cancerous changes can be initiated without any obvious extraneous influence. Our long-term aim with this research is to develop a clinical test to pick up these events.
In mice, telomerase deficiency results in a segmental progeria that increases in intensity over the generations, as the telomeres grow shorter; in humans, similar mutations can result in the syndrome known as dyskeratosis congenita, whose symptoms include bone marrow failure. Mismatch repair defects results in increased cancer incidence (in humans, especially colon tumors). Both types of mutation dramatically decrease lifespan.
In combination, however, these mutations actually improve longevity.
We’ve seen numerous examples of tradeoffs between tumor prevention and tissue regeneration, usually in situations where increased activity of a tumor suppressor resulted in diminished regenerative capacity. Here, however, we see a case where two different antitumor mechanisms 'cancel each other out' to give both improved tissue regeneration and diminished cancer risk. How many other winning combinations are hiding out there?
A number of companies are forging ahead with the development of telomere-based therapies; a large part of that work today, and a lasting benefit whether these companies succeed or fail commercially, is figuring out just what is going on inside our cells as we age.