-- Eugen* Leitl <a href="http://www.lrz.de/~ui22204/">leitl</a>
______________________________________________________________
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---------- Forwarded message ----------
Date: Fri, 10 Aug 2001 11:08:05 -0700
From: DS2000 <ds2000@mediaone.net>
Reply-To: isml@yahoogroups.com
To: isml <isml@yahoogroups.com>
Subject: [isml] Genetic discovery has implications for cloning, cancer
>From CNN,
http://www.cnn.com/2001/HEALTH/08/09/dna.switch/index.html
-
Genetic discovery has implications for cloning, cancer
August 9, 2001 Posted: 3:19 PM EDT (1919 GMT)
NEW YORK (CNN) -- A newly discovered genetic process offers tantalizing
clues for cancer researchers and reveals possible obstacles to cloning,
scientists report.
Results show that despite the success of mapping the human genetic code --
the human genome -- it is only a first step in understanding how genes work.
Four articles in this week's Science magazine detail how genes in human DNA
appear to be controlled by a sea of surrounding proteins that functions as a
master switch.
Molecular geneticists call the newly discovered process the 'histone code'
and say they are just beginning to translate it.
The articles describe methylation, a chemical process that acts as a
trigger. Scientists have watched the common organic molecule methyl interact
with the proteins surrounding DNA, and say the cell appears to use the
process to switch blocks of genes on and off.
The discovery may be a new argument against human cloning. Even with the
right cell and the right DNA, until scientists understand "this parallel
rule book of genetics," they cannot clone without error, said researcher C.
Davis Allis at the University of Virginia, who worked on the projects.
Surrounding DNA with the wrong histones could trigger tumors or
developmental problems, he said.
The discovery also complicates the understanding of genetic disease, Allis
said, because it means a faulty gene alone may not be to blame for a medical
condition. The protein neighborhood that surrounds the gene may be at fault
instead.
Learning how to manipulate the histone code is key, Allis said. "If we knew
how to control which genes we want to turn on or off, we might be able to
reduce disease risk," he said. "For example, we could turn off genes that
promote tumor growth to help prevent cancer development, turn on other genes
that suppress tumors."
The work was done in four labs by researchers at the University of Virginia,
the National Institutes of Health, Cold Spring Harbor in New York, and
Vienna, Austria.
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