Discoveries by Nobel laureate Carol W. Greider and her colleagues have led to advances toward potential cures or treatments for certain types of cancer, and for a growing list of diseases rooted in malfunctions of the DNA-protecting enzyme, called telomerase, that she discovered.
In cancer, the overproduction of telomerase enables tumor cells to maintain unchecked reproduction, and researchers are trying to inhibit the telomerase as a way to shut down the tumor and allow it to die. One experiment involves a potential vaccine to battle runaway cell division in metastatic breast cancer.
Other disorders appear to be caused by underproduction of telomerase. For example, Greider and colleagues at the Johns Hopkins University have developed a mouse model for a rare and fatal inherited disorder called dyskeratosis congenita. Victims cannot maintain production of stem cells in bone marrow because of a shortage of telomerase.
"There are various strategies related to telomerase in clinical trials now," said Jeremy Berg, director of the National Institute of General Medicine, part of the National Institutes of Health. "It's a novel approach, and in principle it should have beneficial effects. But until you do studies in humans, you never know how it's going to turn out."
None of these hopeful implications for human health could have been predicted 25 years ago when Greider discovered telomerase while working as a graduate student in the lab of Elizabeth Blackburn, then at the University of California, Berkeley. She was studying chromosomes, which carry the strands of DNA that hold the instructions for human cell development.
"We were just curious to know how it is that the chromosomes can be maintained, when we knew [they] should shorten over time. We didn't know at the time there were any particular disease implications," Greider, 48, said Monday.
She spoke at Johns Hopkins Hospital, where she is director of molecular biology and genetics at the Institute for Basic Biomedical Sciences. She shares her Nobel Prize with Blackburn, now of the University of California, San Francisco, and Jack Szostak of Harvard Medical School.
By 1984, Blackburn and Szostak had already demonstrated that simple, repeated DNA sequences - which they dubbed telomeres - made up the ends of the chromosomes, stabilizing them from damage during cell division.
