Re: AGING/A4M update

Joao Pedro de Magalhaes (joao.magalhaes@fundp.ac.be)
Tue, 14 Dec 1999 14:36:22 +0100

Hi!

You wrote:
>If the trials work out, it will be interesting because I am guessing
>that when Geron produces a telomerase inhibitor it could well be
>a "ho-hummm" in the market if these drugs are out first. Its good
>from our perspective, because it means we have now have a bi-modal
>approach to the Hayflick Limit and cells that have broken through it.
>You give people gene therapy with telomerase to promote cell division
>in cells that have stopped due to telomere loss (such as endothelial cells),
>then inhibit the development of any large tumors with the angiogenesis
>inhibitors. Previously I was always uncomfortable with telomerase because
>giving them telomerase would seem to be a necessary, but tumor
>promoting approach that would have to be followed by giving them
>a telomerase inhibitor to block any cancer that was started or
>accelerated. Now we have a way around that.

I didn't know you were such a big fan of the telomerase theory! However, the truth is that, unlike the free radical theory, the telomerase theory is a cellular, in vitro, theory, not an organismic one. Also, don't you think research based on Hayflick's limit (as most telomerase research is) can be biased? How do you explain that cells taken from species that appear not to age also follow Hayflick's limit and also have a latent period in accordance with donor age. In addition, there is evidence indicating that telomerase is not the only enzyme controlling telomere lenght.

Anyway, I'm just curious and decided to post my once-every-six-months e-mail.

Hasta.

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