Salk Non-Resident Fellow Honored With Nobel Prize For The Discovery of Telomerase

Elizabeth H. Blackburn, PhD, a professor at the University of California in San Francisco and a non-resident fellow at the Salk Institute for Biological Studies since 2001, will receive this year’s Nobel Prize in Medicine/Physiology for “the discovery of how chromosomes are protected by telomeres and the enzyme telomerase,” the Nobel Foundation in Stockholm, Sweden has announced.

 

The Nobel Foundation will present its prestigious prize to Blackburn in Stockholm during a formal ceremony on December 10. Blackburn shares the award with Carol W. Greider, PhD, a professor at Johns Hopkins University School of Medicine and Howard Hughes Medical Investigator Jack W. Szostak, PhD, a professor at Harvard Medical School. 

 

“The discovery of telomerase and the role telomeres play in human biology by Salk non-resident fellow Elizabeth Blackburn and her colleagues undoubtedly opened a new door for cancer research while also deepening our understanding of the aging process,” says Salk president William R. Brody. “We applaud their contributions and the impact they are having today toward the development of treatments to improve the human condition.”

 

Telomerase activity is now known to be the main mechanism by which human tumor cells achieve immortal growth. Cancer cells are “addicted to telomerase,” as Blackburn likes to put it, and reducing the quantity of telomerase will halt the division of cancer cells in their tracks. Not surprisingly, telomerase has become a prime target for novel therapeutic cancer intervention, and several clinical trials for telomerase based cancer therapy are already underway.

 

“Today’s award celebrates the achievements of three profoundly creative scientists, who solved a very fundamental question about the ends of chromosomes. Their pioneering work, performed in two simple experimental organisms — a ciliated pond organism and baker’s yeast — laid the groundwork for current research on the role of telomeres in cancer and human aging,” says Vicki Lundblad, PhD, a professor in the Molecular and Cell Biology Laboratory.

 

Blackburn, Greider, and Szostak provided the solution for a long-standing biological puzzle better known as the “end replication problem”: Each time a cell divides, it has to faithfully duplicate all its chromosomal DNA so that each daughter cell receives a complete set. The problem with this crucial process is that the replication machinery cannot copy linear chromosomes all the way to the tip. This led to the prediction, more than 30 years ago, that without some additional mechanism to continually replenish the very tips of chromosomes, the ends would slowly whittle away, and the cells left to perish.

 

Even as early as the 1930s and 1940s, scientists had suggested that chromosome ends were capped by special structures, so-called “telomeres” from the Greek for “end” (telos) and “part” (meros) that would protect these fragile ends. But it was not until 1978, when Blackburn — with the help of the tiny pond-dwelling ciliate Tetrahymena — discovered that telomeres consist of a short, simple DNA motif repeated over and over again, that the precise makeup of telomeres was determined.