Telomeres on metaphase chromosomes in normal human fibroblasts, visualized using digital fluorescence microscopy.

 From the laboratory of Drs. Jerry W. Shay and Woodring E. Wright.

We must better understand the function of the telomeric complexes in balancing cell proliferation and tissue renewal against the risk of cancer

- Emmanuel Skordalakes


For almost half a century bioscientists have known there’s a strong natural barrier that prevents immortality – most of the time. An intriguing, important clue came from Leonard Hayflick, decades ago when he was at Stanford University. Hayflick determined that cells growing in culture can only keep dividing through about 50 doublings before they fall into senescence and stop growing. That also seems to be true in vivo.

An important part of this genetic timing mechanism seems to be the telomere, a DNA-based structure that decorates the tip ends of each chromosome. Research has shown that each time a somatic cell divides all of its telomeres lose a little bit of length. They keep getting shorter until they get so small they shut down cell division, inducing cell senescence. There seem to be several reasons for this. First, if a cell can’t become immortal, it can’t become cancerous. Second, telomere shortening serves as a clock, a timing mechanism that tells a cell how old it is. And third, telomeres contribute to genome stability by keeping chromosomes from being scrambled.

But there’s also an enzyme called telomerase, which rebuilds telomeres in stem cells, allowing them to keep on dividing indefinitely for the sake of reproduction and wound repair. And telomerase is also “turned on,” perhaps accidentally, in cancer cells, which exploit immortality – with lethal results.

Thus research into telomeres, telomerase, their relationships, activities and impacts is one of the hottest areas of biomedical research, being important in aging, cancer, and genome science. The Ellison Medical Foundation is a major contributor to this effort.


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