From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Sun Sep 14 2003 - 14:55:57 MDT
On Sun, 14 Sep 2003, Aubrey de Grey wrote:
> All I have time to say right now is that there is a way out of the
> "mess" that Robert describes, which is outlined at:
>
> http://www.gen.cam.ac.uk/sens/SENS3.htm
Aubrey, my readings right now suggest that the ALT pathway for
the extension of telomeres (or at least part of the ALT pathway)
involves homologous recombination repair between telomeres. It
makes sense since telomeres are essentially identical and so
it is difficult to prevent short telomere from using a longer
telomere as a repair substrate. If so it is going to be hard
to deal with -- one has to suppress homologous recombination
DNA repair in pre-cancerous cells. Not impossible mind you but
pretty darn difficult. One would presumably turn down the
ability to do homologous recombination repair system as the
telomeres shorten. But I suspect there will be tissues where
that has a significant negative impact (in terms of cell replacement
capacity). One of the problems is that we don't fully understand
the degree to which telomere extension needs to be tuned
for specific tissues based on their cell division rate.
I suspect the optimal balance between telomere extending
and shortening is not attained in many tissues.
So while I agree that there may be a partial path out of the "mess",
I think we still have a lot more to learn.
On a positive note, though I can't discuss it, Juvensa may be on
the path towards a "homologous recombination-based gene therapy"
approach that may be workable. If that plays out in a successful
way you will have a much greater toolbox to work with.
Robert
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