Why They Got the Nobel Print E-mail



Wendy Wolfson
Newswire21.org

The three researchers who received this year's Nobel Prize for Medicine got it for giving insights into cancer and aging at the most basic cellular level. But the importance of their work in the arcane world of telomeres and telomerase may have been lost amid all the hoopla.

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Telomeres (pronounced tee-loh-meers) are protective caps on the ends of chromosomes in cells. Chromosomes carry genetic information, so it is important that they are precisely copied in cell division.

Telomerase (teh-LAH-meh-race) is an enzyme that keeps restoring the ends of telomeres as cells divide, enabling the entire chromosome to be copied intact. But this process goes awry in cancer.

Dr. Elizabeth Blackburn, a  biochemistry professor at the University of California, San Francisco; Carol Greider, a Ph.D. of  Johns Hopkins School of Medicine, and Jack Szostak, a Ph.D. at Harvard Medical School and a researcher at Howard Hughes Medical School, were awarded the prize for their work  in the 1970s and 1980s on telomeres' fundamental roles in cell division and death.

"The question of how cellular aging relates to abnormal cell division, such as cancer and the aging of organisms continues to be the focus of rigorous study, thanks to the insights of Drs. Greider, Blackburn, and Szostak," said NIH Director Francis Collins, in a statement released the day of the Nobel announcement.

Telomeres don't contain any genetic information, just the same sequence of DNA bases repeated several thousand times. But they act like aglets, those plastic sleeves that prevents shoelaces from fraying, to protect the chromosomes as cells divide.  

Blackburn and Greider discovered that the enzyme telomerase is active in the cells of babies in the womb but shuts off by kindergarten. This means that as cells divide, the ends of the chromosomes are not completely copied. The older we get, the more our telomeres wear down.

Stress Impacts
In a 2007 New York Times interview, Blackburn said that chronic psychological stress, like caring for a family member with dementia, can also accelerate telomere wear and tear. And low telomerase is linked to stress-related illness. 

Scientists think that when the telomeres get too short to function properly the cell stops dividing. By looking at the length of a chromosome's telomere, researchers can gauge how many times a cell has divided, and how far it can go before it stops replicating itself.

At least, this is how it is supposed to work. But in advanced cancer, telomerase is active, enabling cells to keep dividing ad infinitum and the telomeres at the tail end of chromosomes don't shorten with each cell division.

The work of the trio has spurred initiatives to find vaccines and drugs that could inhibit telomerase enzyme in cancer, as well as research into certain genetic diseases that are caused by defective telomerase, such as congenital aplastic anemia and certain hereditary skin and lung diseases.

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