Within each and every one of your trillions of cells sits a molecular hour-glass. The time when each and every cell must stop dividing comes closer with every grain of sand that drops through this tiny clock.
The grains are letters of DNA code that fall off these cellular timepieces. Scientists call them telomeres and there is good evidence that they go wrong in cancer so that, by fixing them, tumours could be made to expire on schedule. Earlier this month, a team in California managed to inhibit the spread of melanoma skin cancer by exploiting this mechanism.
Longer life for your cells is not necessarily a good thing - cancer cells are an immortal machinery run amok, for example; an ultimately fatal hazard to finely tuned biochemistry that depends on cellular turnover and lifecycles. The melanoma research mentioned above is worth further reading if you are interested in seeing a facet of telomere research in action:
In the study, researchers found through gene expression profiling in mice that eight genes involved in glucose metabolism were lowered when telomerase was suppressed in skin cancer cells. The result was a return of pigmentation, frequently absent in advanced melanomas, and of cancer cells losing their metastatic potential.
"We introduced a telomerase inhibitor into melanoma cells and found that by suppressing telomerase, melanoma cells start to change," said Kashani-Sabet. "In some melanomas, pigmentation is lost. We found that when we are able to shut down telomerase, the cells regain functions previously lost, such as the ability to make pigment."
"As the cells become too acidic from the buildup of lactic acid, the proteins that control pigment production can be turned off, suggesting that glucose metabolism plays a key role when combined with telomerase in metastasis."
Shutting down metastasis is a very big deal in cancer treatment. A range of other telomere-related strategies are presently under exploration for the prevention or treatment of cancer. Unlike past generations of research, these are carefully tailored approaches based upon ever more accurate knowledge of the biochemical mechanisms at the root of cancer.
But what of telomeres and aging? From the Telegraph article:
Others believe that telomeres may hold the key to ageing itself. A team at Brown University in Rhode Island recently reported that cells with faulty telomeres made up about four per cent of connective tissue in five-year-old baboons. But in 30-year-olds, that number rose as high as 20 per cent, providing evidence to support the theory that old cells help make old bodies.
When telomeres run out, cells become "senescent". Under a microscope, they look bloated. Analyse the way that they use genes and one can see changes that make the senescent cells secrete factors that make tissues deteriorate. Because they hang around for years, rather than do something helpful like die, these old cells may well underpin age-related disease.
Perhaps a way to turn back telomeres can be found, marking the culmination of the search for the elixir of youth, although there is still a great deal of argument about whether it is ageing that shortens telomeres or whether stubby telomeres cause ageing.
The argument will be solved by further research - there are convincing positions on both sides, for all the original form of the telomere theory of aging has been largely abandoned. It seems clear that aging has many more contributory causes, and it is far from decided as to where shortened telomeres fit into the picture - other than as a cause of cancer, that is, where the science is as definitive as it gets in an very active field.
Amongst the research groups who see therapies for the root causes of degenerative aging emerging from telomere science are young companies like Phoenix Biomolecular, Sierra Sciences and Telomolecular. You should take a look at what they have to say about their areas of research.