excelife at earthlink.net
Sat Aug 1 15:21:29 EST 1998
In article <35C27767.DE2 at netcom.ca>, tmatth at netcom.ca says...
>> A Medline Search comes up with over 160,000 papers including the
>> phrase "growth factor".
>> I've reviewed a number of articles and read the abstracts on a small
>> of these papers and some very exciting work is going on.
>After all, it does not take many doublings of *all* of a bunch of cells
>to create a *lot* of usable tissue. So maybe the tissue will then have a
>smaller telomeric lifespan potential that other comparable body tissue,
I expect that 99.999% of
>them never even concerned themselves about telomeres at all.
Thanks to you, Dr. Ames and a number of other people this research is finally
coming into better focus for me. As I see it then, many of these growth
factors are part of the normal cellular maintenance, regulatory and
As Dr. Ames pointed out trauma to epidermal cells will cause the remaining
cells to release some growth factor, possibly transforming growth factor beta
2 or 3. This initiates mitotic division to produce cells to replace those
lost to the trauma and then another growth factor regulates the
differentiation of the daughter cells into the various cell types making up
Apparently then, Genzyme and Advanced Tissue Sciences are taking these growth
factors, applying them to epidermal cells in vitro and "tricking" them into
reproduction since they have received the chemical indicator of trauma.
Following Toms' reasoning, the inability to grow skin cells in vitro earlier
wasn't that they had hit their "Hayflick Limit" but rather because it took to
long for them to replicate. The growth factors are able to overcome this
limitation as mentioned above. However, since they may not be having any
effect on the telomeres then their potential replicative capacity may be
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? 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?
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. 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.
These are just some ideas but I hope they suggest some possibilities for
combining the work on growth hormones with that on telomeres and telomerase.
Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
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