The answer is obvious:

If we can turn off telomerase production, then we should also be getting close to turning on production of telomerase. Stem cell telomeres are much longer than cancer cell telomeres, and thus should still be intact long after the cancer cells are dead. It may still be a dream to lengthen the telomeres to stop aging, but it is an exciting possibility.

Since telomerase is ultimately under the control of the telomerase gene, much research has been taking place in the genetic aspects of this problem. The range of activity is virtually unlimited: experiments with bacteria, with yeast, with other single celled organisms; experiments on insects, rodents, and humans; and the ever-present statistical analyses.

Some studies done at the University of California by Dr. E. H. Blackburn have involved the use of single celled organisms called ciliates (Tetrahymena thermo-phila), as well as the yeast, Kluvyeromyces lactis.

By causing mutations in the template sequence of telomerase RNA, researchers were ultimately able to show that:
"...a crucial determinate of telomere length homeostasis is the nature of the duplex DNA--Rap 1 protein complex on the very end repeat of the telomere. We propose that this complex plays a complex role in regulating access of telomerase to the telomere."

This suggests that it is the molecular makeup at the outer tip of the telomere that plays a large role in the telomere maintaining its length during cell division, adding yet another piece to the puzzle.

With all the pieces of the puzzle in place, there is also little doubt that it will be accompanied by a huge extension to the human life span. And who knows, perhaps even more.

[Dr. McLeod and Dr. White anticipate with enthusiasm the next symposium on telomerase research.]