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The potential to learn more about aging, longevity determination and the
diseases of old age by studying cultured normal and cancerous human cells
is enormous. Here are some examples of present research directions:
The reason that cancer
cells are immortal is that, unlike normal cells, they produce an enzyme
called telomerase that maintains their telomeres at a constant length.
This prevents a diminishing length from triggering the cell to stop dividing
as it does in normal cells. Because telomerase is found almost exclusively
in cancer cells, a search is on for chemical inhibitors of telomerase.
An inhibitor, if found, could be useful in preventing the further replication
of cancer cells.
In a discovery made
two years ago, it was demonstrated that normal mortal human cells could
be made immortal by using a procedure that made the normal cells switch
on the production of their telomerase enzymes. These normal human cells
became immortal yet still retained their normal properties. The potential
use of this technique is great, making it possible to produce normal human
cells on a large scale and enabling the cells themselves or the products
they produce to be used for a variety of therapeutic purposes.
Tests being developed
for the presence of telomerase are so sensitive that single cancer cells
can be detected in body fluids like urine and saliva. This could provide
opportunities for much earlier detection of bladder and lung cancer cells.
Telomerase expression in cancer cells is the single most specific difference
yet found between normal and cancer cells.
The goal of research on the phenomenon of cellular senescence is not
unlike the goal of all research on the biology of aging. It is not to
make us all immortal; that is not only impossible but also undesirable.
Nor is it to stop or slow down the processes of aging, because those processes
are inevitable. And because the determinants of our longevity are driven
indirectly by most, if not all, of our genes, it is also very unlikely
that tampering with that process is either probable or even desirable.
Instead, our goal in this research and other research in the field of
aging should first be to understand why old cells are more vulnerable
to disease than are young cells. Once accomplished, those differences,
if exploitable, could result in a maximum 15-year increase in human life
expectation. Then the underlying inexorable processes of aging will be
revealed as the cause of death. Unfortunately, those processes, absent
the replacement of all vital organs--including the improbable replacement
of the brain--will almost certainly be inescapable.
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