Cancer | haltagingnow

The Cancer Problem

You might be wondering why biologists don't simply find a way to keep our body's telomeres long. This would prevent replication errors and humans could live indefinitely. The big problem is cancer. Usually, if a cell makes an error in copying itself, the error will prevent the cell from duplicating itself in the future. So the mistake is limited. But with cancer, cells with errors somehow "turn on" the production of telomerase and make the mutant cell immortal. Now, aberrant cells can reproduce unchecked and outlive normal cells. This is the process that creates tumors.

Since we all have mutant, pre-cancerous cells in our bodies, nature has decided to shut off the telomerase as we age, thus preventing these mutant cells from growing telomeres. It's a kind of programmed death -- a trade-off to reduce our lifespan in order to save us from being riddled with tumors. Nevertheless, some pre-cancerous cells manage to re-activate their telomeres and this has caused the research to focus more on blocking telomere production rather than trying to extend it.

The molecular structure shows an interesting "groove" (show in green) where the enzyme attaches to the end of the DNA molecule.

Anti-cancer researchers believe that by introducing a molecule to block this groove, the telomerase would become unable to attach itself to the DNA and thereby limit the length of telomere production. While this work holds hope for stopping tumor cells from reproducing forever, it does little to extend healthy cells from being rejuvenated. However, if the molecular "blocker" could specifically target only cancerous cells, without blocking telomerase activity in healthy cells, it could be a step towards human life extension if and when a pharmaceutical can be developed that activates telomerase in the human body.

The telomere hypothesis of cancer is that the function of telomere shortening is to cause cells that have lost normal control over growth to senesce (i.e. stop growing) before being able to replicate enough times to become a tumor, thus decreasing the frequency of cancer.

Immortal cells like cancer have an unfair advantage over normal human cells which are designed to senesce. But nature seems to have planned this human telomere shortening perhaps to prolong life by hindering the otherwise unchecked growth of non-immortal or benign tumors. Malignant, or immortal tumors can simply outlive the rest of the organism.

Malignant cancer cells are being studied because they appear to have altered the shortening of telomeres by turning "on" the telomerase. Thus it appears that some cancers and aging are both connected with the biology of telomeres.

It is possible that increasing telomerase activity in normal cells might stop the biological clock of aging, yet the side effect of this intervention might be an increase in the rate of cancer. Further understanding and refinement in the telomere hypothesis might lead to a way to slow the aging process and prevent or arrest cancer.

However telomeres function, they are an integral part in the very complex process of cell growth, involving many other factors as well. Telomerase might be the Achilles Heel of aging and cancer, but as our understanding of factors that interact with telomerase, factors that are responsible for telomere shortening in the first place, and non-telomerase mechanisms for increasing the length of telomeres, we might find that one of these factors is more easily manipulated to slow aging or prevent cancer. Also there are additional factors that affect aging and cancer, which might prove in the end to be more important than telomeres and telomerase.