wonderful news

From: Eduardo Blasina (blasina@adinet.com.uy)
Date: Tue Jan 13 1998 - 19:01:50 MST


Adds quotes, reaction)
   By Maggie Fox, Health and Science Correspondent
   WASHINGTON, Jan 13 (Reuters) - U.S. scientists said on Tuesday they had
been able to make human cells live longer by tinkering with their genetic
material, providing a "fountain of youth" for aging cells.
   The findings, published in the journal Science, offered hope of new ways
to treat diseases such as cancer.
   "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," Dr.
Woodring Wright, a professor of cell biology at the University of Texas in
Dallas, said in a statement.
   "This is a monumental advance in the understanding of the molecular
genetics of aging," Leonard Hayflick, professor of anatomy at the
University of California San Francisco and the discoverer of human cellular
aging, said in a statement. "The telomerase gene will likely have many
important applications in the future of medicine and cell engineering."
   News of the technology sent shares in California-based biotechnology
group Geron Corp. <GERN.O> up four points on the NASDAQ stock exchange.
   "We believe that the extension and perhaps immortalization of human cells
will have many important applications for the treatment of age-related
diseases," said Calvin Harley, chief scientific officer at Geron.
   Wright and colleagues at the university's Southwestern Medical Center,
who worked with Geron, used an enzyme known as telomerase. Produced by germ
cells such as eggs and sperm, it affects the ends, or telomeres, of the
chromosomes which carry the genes.
   Normal cells do not produce telomerase. Every time a cell divides it
loses a little bit of the telomere on either end of the chromosome. Wright's
team found a way to make the telomeres grow back using the enzyme.
   "Each time a cell divides its telomeres get shorter and shorter and
shorter," Wright said in a telephone interview. His team proved last year
this loss was associated with aging.
   Now, they said, they proved you can stop the aging process, at least on a
cellular level.
   "Unequivocally I would say this would not allow you to live forever,"
Wright said. "This is not going to be a pill that allows you to live longer
any time soon."
   He said the the natural process that kills off cells was just one
component of aging. "It's possible that just like when you have a car and at
80,000 miles you replace the engine -- you haven't made that car immortal.
On average the car is going to run longer but then the transmission is going
to go out or the brakes or something else."
   But the finding could help individual cells live much longer. "Over time
we hope this will have significant effects on the health span and eventually
on lifespan," Wright said.
   Wright's team used skin cells, cells from the retina in the eye and skins
from inside arteries. All were able to grow back their telomeres and did
not, as normal cells do, eventually stop dividing and die.
   "They are still dividing," Wright said. They were also normal, showing no
sign of becoming cancerous.
   "I think the medical implications of this work are really profound," said
Dr. Jerry Shay, who worked with Wright. "It will allow us now to take a
person's own cells, manipulate and rejuvenate them without using up their
own lifespan, and then re-inject them."
   In other words, it could be the break that gene therapists have been
looking for.
   Gene therapy involves taking the cells of a person with a genetic disease
such as cystic fibrosis, inserting the healthy gene and then putting the
cells back in the patient in the hope that the manipulated cells will take over.
   But the engineered cells are old by the time the scientists are through
with them and often die off before they can do much good. Wright hopes the
telomerase process can make the cells immortal and make them work better.

Tuesday, 13 January 1998 22:08:48
RTRS [nN13216863]



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