Excelife excelife at
Sat Aug 1 15:21:29 EST 1998

In article <35C27767.DE2 at>, tmatth at says...
>Excelife wrote:
>> 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.
>Tom Matthews

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 
reproductive systems.

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 
the skin.

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.

Any thoughts?

Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.

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