Study shows how 'fountain of youth' enzyme works

By Maggie Fox, Health and Science Correspondent

WASHINGTON, March 29, 1999 (Reuters) - Scientists said on Monday they
had
made some surprising discoveries about how an enzyme helps cancer cells
become immortal.

Their findings could not only help doctors better understand cancer, but
could
help researchers trying to create long-lived cells for research and for
eventually growing tissues to treat disease.

The study involved telomerase, an enzyme that is known to help cells
live longer. It stops the fraying of telomeres -- the caps on the end of
chromosomes, which get shorter and shorter every time a cell divides.

``What this study did, it showed a real Jekyll and Hyde characteristic
for telomerase,'' Elizabeth Blackburn, a professor of cell biology at
the University of California San Francisco who led the study, said in a
telephone interview.

Normally, a cell can divide between about 50 and 80 times before its
chromosomes, which carry the DNA, start getting tattered. In a healthy
cell, the telomeres send a message saying they are worn to a nub, and
the cell will die.

Telomerase can extend a cell's life, preventing this natural process. It
is known to be involved in cancer, in which cells start an
out-of-control growth that becomes a tumor.

But telomerase can also be used to grow immortal ``cell lines'', which
are cultures of cells that scientists can study.

Lately, researchers have been trying to grow cultures of stem cells,
which can give rise to a number of different kinds of tissue. Such
tissues might be used in transplants, perhaps to treat diseases ranging
from Parkinson's to diabetes.

These scientists had assumed that telomerase just re-built the
telomeres, effectively giving a cell new life.

Not so, Blackburn's team wrote in a report published in the Proceedings
of the National Academy of Sciences.

``That was the surprise,'' she said.

They infected human cells with SV40, a monkey virus known to cause
cancer. They then exposed them to TERT, a human protein that activates
telomerase.

The telomeres continued to wear down with each cell division. But the
cells did not die on cue.

``Normally, cells get an alarm signal from the telomeres saying 'stop
dividing, stop dividing','' Blackburn said.

With exposure to telomerase, the cells seem to get a little cap on the
chromosomes, protecting the telomeres and stopping that signal.
``Eventually they bottom out, but at much, much shorter lengths than
would have been expected,'' Blackburn said.

This is both good news and bad news for health.

``Here's the bad news. The cells that we were using were not really
nice, well-behaved cells,'' Blackburn said. ``They had been transformed
with a virus whose job is to turn off safety devices that normally
protect against cancer.''

With the help of telomerase, such cells could spread cancer in the body.

But the good news is that normal, healthy cells exposed to the
telomerase also continued dividing -- which would help researchers
trying to create immortal lines of stem cells for research.

Cells exposed to an inactivated form of telomerase did not become
immortal, even when they had also been ``activated'' by the SV40 virus,
Blackburn said.

Blackburn said her team found much the same process happened in yeast --
which not only shows that yeast is a useful tool for studying human
cancer, but that the process is one that is basic to biology.

Copyright © 1999 Reuters Limited.
--
Judith Richards, London, Ontario, Canada
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