tmatth at netcom.ca
Sat Aug 1 20:19:05 EST 1998
> This raises some intriguing thoughts. Is it possible for, for example, that
> slow growth cancers like some seen in the prostrate are the result of
> telomerase activity alone?
No. Every cell also is inhibited from dividing by mechanisms which sense
that it is surrounded by neighbors. One of the requirements for a cell
to become cancerous and start duplicating to from a tumor (even slowly)
is that it lose this inhibiting ability.
> The cells would be immortal and increasing in
> cellular mass but since they are only replicating at the normal rate the
> cancer is slow to grow. Whereas highly prolific cancers may have both a
> telomerase component allowing unlimited growth and a growth factor component
> causing the cells to multiply rapidly?
Certainly the differences are due to growth factors or promotors of some
kind if only hormone membrane reception.
> Or in a clinical setting, assuming both telomerase and the growth factors can
> be adequately controlled, a person with a diseased liver wouldn't be helped
> by telomerase alone since the cells probably wouldn't replicate fast enough
> to make a difference.
I think it is true that there are many kinds of cancers which don't rely
much or at all on telomerase and thus won't be stopped by any
> Similarly growth factors alone might be able to
> replace the lost cells but their replicative capacity might be too short for
> the process to be effective over a long period of time and the liver
> dysfunction would return. Together, however they might be able to restore
> the lost cells quickly and continue to be viable over the long run.
Don't forget that the liver is special, being the only major organ that
I am aware of which can regrow itself to normall mass from a small
healthy piece without any special intervention. In doing so, presumably
it is reducing the replicative life-span of the new cells, so that the
new liver is "replicatively older" than an unregenerated liver would
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