One basic quality of human life is that every time our cells divide the tips of our chromosomes get shorter. This shortening of telomeres may be the molecular clock of aging. Indeed, the shortening of telomeres has been shown to be the trigger that induces senescence of human cells grown in culture; whether this can be extrapolated to include human organismal aging itself is not yet known. The correlation between telomere length and age is very strong and shorter telomeres directly correspond to shorter human life expectancy, but "cause and effect" are still debated. Finding ways to prevent telomere shortening could be an ideal way to address these issues and answer the question once and for all: Does prevention of telomere shortening extend our lifespans?
It is unfortunate that anything that is done to extend the lifespan of our cells will also extend the lifespan of our cancer cells. Excision of the telomerase gene and genes involved in the "Alternative Lengthening of Telomeres" (ALT) pathway is one way to overcome this cancer issue. But our lifespan will be limited more than ever by the length of our telomeres. This leaves us with the irrefutable conclusion that we will be unable to significantly extend our lifespans without finding a cure for cancer that doesn't limit our ability to extend the lengths of our telomeres.
In hopes that the cure for cancer will be forthcoming, several biotech organizations and academic institutions have accepted the challenge of finding ways to prevent telomere shortening by transiently inducing the activity of telomerase. The purpose of this presentation will be to review the current progress, including the recent discovery of several small molecules that induce telomerase activity in normal human cells.