September 18, 2006

UCSF's Blackburn Wins Lasker Award for Basic Medical Research

Elizabeth Blackburn

Molecular biologist Elizabeth H. Blackburn, PhD, has been named to receive the prestigious Lasker Award for the prediction and discovery of telomerase, a remarkable enzyme that synthesizes telemores, the tiny units of DNA that seal off the ends of chromosomes, protecting them and maintaining the integrity of the genome. Blackburn shares the award with Carol W. Greider, 45, of Johns Hopkins University School of Medicine and Jack W. Szostak, 53, of Harvard Medical School. Blackburn, 57, is the Morris Herzstein Professor of Biology and Physiology in the Department of Biochemistry and Biophysics at UCSF. The Lasker Award has been given to 71 scientists who subsequently went on to receive the Nobel Prize. The awards will be presented at a luncheon ceremony on Sept. 29 at the Pierre Hotel in New York City. In 1975 to 1977, as a postdoctoral fellow at Yale University with Joseph Gall, PhD, the recipient of the 2006 Lasker Special Achievement in Medical Science Award, Blackburn discovered the unusual nature of telomeres (TEEL-oh-meers). The work was published in 1978. In 1985, while a professor at University of California, Berkeley, she and her then-graduate student Greider reported the discovery of telomerase (tel-AH-mer-AZE). Blackburn, who moved to UCSF in 1990, had determined while at Berkeley that, in some organisms, such as the single-celled pond dweller tetrahymena, telomerase continuously replenishes the telomeric tips of chromosomes. In humans, however, others including Blackburn and her group subsequently showed that it is damped down at certain times in the life of many types of cells, limiting their ability to self-replenish throughout life. The scientists were honored for their groundbreaking investigations in the late 1970s and 1980s. In addition to providing insight into how chromosome ends are maintained, their work laid the foundation for studies that have linked telomerase and telomeres to human cancer and age-related conditions, such as cardiovascular disease. "This basic research had no medical impact for 15 years - until the early 1990s - when scientists identified telomerase in human cells and showed that it played a crucial role in two disease-related areas: cancer and aging," said international jury chairman Joseph L. Goldstein, a recipient of the 1984 Lasker Award for Basic Medical Research and the Nobel Prize in Medicine in 1985. "Today, telomerase research is one of the hottest fields of biomedical science." Blackburn's laboratory at UCSF Mission Bay focuses on telomeres, which play a critical role in determining the number of times a cell divides, its health, and its life span. They do so through a curious phenomenon of nature: Each time a cell prepares to divide, a portion of the telomeric DNA erodes away from the tips of chromosomes and, after some tens of rounds of cell division, when a certain amount of telomeric DNA has gone, the cell stops dividing, ages and dies. This process affects the health of cells and the tissues they form. In discovering the telomerase enzyme, Blackburn determined that in some organisms, such as the single-celled pond dweller Tetrahymena, the telomerase enzyme continuously replenishes the tips of chromosomes. In humans, however, it is damped down at certain times in the life of many types of cells, limiting their ability to self-replenish throughout life. Today, scientists are exploring whether the telomerase enzyme could be reactivated to prolong cell life - in order to treat age-related and neurodegenerative disorders ranging from skin wrinkles to blindness to cardiovascular disease - and deactivated to treat cancers, in which, the enzyme is usually abnormally overactive. Broadening the scope of the research in recent years, Blackburn, who moved to UCSF in 1993, and UCSF colleague Elissa Epel, PhD, have reported that chronic psychological stress and the perception of life stress, take a toll on telomeres and telomerase. The findings have implications for understanding how, at the cellular level, stress may promote earlier onset of age-related diseases.

Related Links: