From: Brett Paatsch (paatschb@optusnet.com.au)
Date: Mon Jun 23 2003 - 23:21:34 MDT
In the article below it seems the myc cancer causing gene
(which is already known to be responsible for about a third
of all cancers (bad gene, very bad! ) produces the protein
that activates the Werner's gene (a fine friendly gene, one
warms naturally to it, - because in healthy folk that don't suffer
from the rare premature aging syndrome known as Werners
when the gene is broken) it is actually involved in keeping
cells young and growing.
So, the bummer of it is, the gene that keeps cells young and
growing is fired off by a gene that gives you cancer. Sort of.
Irritating universe. Still it is better to know. As now, maybe,
we can gerry rig some sort of work around or kludge.
Also, we may get some more insight into kicking cancers butt.
------------
Scientists identify genetic link between cancer and aging
http://www.eurekalert.org/pub_releases/2003-06/cshl-sig062303.php
A collaboration of scientists mainly from the Fred Hutchinson
Cancer Center and at the University of Washington (Seattle)
has made an important discovery linking the powerful cancer
-causing oncogene, myc, with the gene behind the premature
aging disease, Werner syndrome. Their finding reveals that the
MYC oncoprotein turns-on Werner syndrome gene
expression, and posits the Werner syndrome gene as a
potentially important participant in MYC-induced tumorigenesis.
Werner syndrome is a rare genetic disorder characterized by
the appearance of old age beginning after puberty. It is caused
by mutations in the Werner syndrome gene (WRN), which
resides on the short arm of human chromosome 8. The WRN
gene encodes a DNA helicase (an enzyme that unwinds DNA)
involved in DNA replication and repair.
..
As Dr. Grandori explains, "We uncovered a role in
oncogenesis for a gene, WRN, whose function was known to
be important in maintaining youth of the whole organism. This
study was prompted by the characteristic ability of tumor cells
in culture to multiply indefinitely and thus to exhibit permanent
youth. Our results are consistent with the hypothesis that
genetic programs that limit organismal aging may, at the cellular
level, promote tumor development, thus constituting a double
sword. On the positive side, we hope that our study will
provide a new therapeutic target able to trigger tumor cells
into senescence."
etc
----------
- Brett Paatsch
PS: "Dr Ray Monnet at the Universtity of washington notes
that "we have recognized deep links between cell senescence
and tumorigenesis for some time. Its gratifying (sic) to see
another of these links identified that is conceptually interesting
and may (sic) have practical importance".
That Dr. Ray has 'scientific detachment' down to an art form.
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