NEW YORK (Reuters) -- For the first time, researchers have confirmed that the
"clock" thought to control aging in human cells does indeed dictate that
process. What's more, they have found a way to circumvent the process --
extending the lifespan of normal, healthy human cells, according to a report
in Science.
The finding has "profound" implications for the study of cancer, which may
use the same process to escape the aging process, according to an editorial
accompanying the study.
And it may lead to treatment for human disease caused by worn out cells, such
as macular degeneration -- the leading cause of blindness in those over 65.
"This research raises the possibility that we could take a patient's own
cells, rejuvenate them, then modify the cells as needed and give them back to
the patient to treat a variety of genetic and other diseases," said senior
investigator Dr. Woodring E. Wright in a statement released by the University
of Texas Southwestern Medical Center at Dallas. "The potential long-term
applications are simply staggering," said Wright, a professor of cell biology
and neuroscience. The study was a collaborative effort involving researchers
at the medical center and at Geron Corp., in Menlo Park, California.
Most cells will divide roughly 50 times in the laboratory before entering a
resting state known as senescence, a process that also occurs in the body.
For more than a decade, researchers have suspected that telomeres, sections of
DNA at the tips of chromosomes, control that process.
Like minutes ticking on a clock, a piece of telomere is lost each time the
cell divides. But some cells contain an enzyme, called telomerase, that can
re-build the telomere after cell division.
In the new study, the gene for telomerase was inserted inside three types of
cells that don't normally carry the enzyme -- retinal pigment epithelial
cells, foreskin fibroblasts, and the vascular endothelial cells -- or those
lining blood vessels. In contrast with cultured cells that have telomere
shortening, the genetically engineered cells continued to vigorously divide
and have long telomeres.
The treated cell population doubled at least 20 more times than normal and
continues to grow, according to the report. The new findings confirm that
telomeres are the "clock" that keeps cells from growing out of control,
according to an editorial by Titia de Lange, of the Laboratory for Cell
Biology and Genetics at The Rockefeller University in New York. And that
mechanism has all "the makings of a powerful tumor suppressor system," de
Lange wrote.
"The results should strengthen the determination of those who are searching
for telomerase inhibitors as potential anti-cancer agents." SOURCE: Science
(1998;279:349-352, 334-335)
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