Telomerase Protein Component Isolated.

Created May 31st, 1997. Copyright 1997 by Duane Hewitt
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The catalytic component of the telomerase enzyme
has been isolated and sequenced . It was isolated from
Euplotes which is a pond dwelling organism with
relatively abundant telomerase.

The Euplotes enzyme sequence was compared to sequences
in the online genetic data banks and demonstrated homology
to reverse transcriptase which is what retroviruses like HIV use
to make a DNA copy of their RNA genome. It had previously
been discovered that telomerase uses an RNA template to
add DNA to the ends of chromosomes. Therefore reverse
transcriptase and telomerase are closely related and similar
strategies may work in inhibiting either of them.

The cancer connection comes in that telomerase is activated
in a majority of cancer cells (85-95%). It is thought that
telomerase activation may be a necessary step for all tumors.
The reason for this is that most cancer cells are "immortal".

Cancer cells, unlike normal cells, can divide indefinitely in
tissue culture if given adequate nutrients. Normal cells have
a limit of 50 +/-10 divisions (Hayflick limit) before they
senesce in culture and stop dividing. The ability of cancer
cells to keep dividing is believed to arise from the activation
of telomerase. Therefore if telomerase is inhibited then the
telomeres in cancer cells will shorten and will act as a brake
on the cancer cell growth (intact telomeres inhibit genes
that block cell growth).

The cancer cells should be susceptible to the telomerase inhibitor
because of the data from the paper that I have referred
to previously. Cancer cells actually have shorter telomeres than
normal cells because they have undergone more divisions
prior to the activation of telomerase. Telomerase activity evolves
in the population of cancer cells because the cells that do not
activate it will die and leaving only cells with telomerase
active in the cancer cell line. Therefore a relatively brief
treatment with a telomerase inhibitor should have dramatic
effects upon tumor growth.

Aging comes into the picture in that the telomeres in your
normal cells are like a clock that is winding down. Each time
the cells divide some of the telomere is lost and eventually you
will not have enough cells to divide and perform essential
tasks and some system will fail. So the prospect arises
for a telomerase tightrope in which cancer cells are inhibited
from dividing and the telomeres in healthy cells are extended
in order to maintain their vitality.