Excerpt: UCSF researchers report that they were
able to slow the growth of human cancer cells - or cause them to
commit suicide altogether -- by creating just a miniscule mutation
in the telomerase enzyme.
The study, conducted in breast and prostate cells grown in
culture and in tumors formed from human breast cancer cells
grafted into mice, suggests that human cancer cells are much more
sensitive to disruptions in the telomerase enzyme than had been
thought. The finding hints, the researchers say, at a possible new
strategy for thwarting human cancers.
In humans, telomerase is inactive in most adult cells, and
only active at certain times in others, but it is highly active in
cancer cells, and has been suggested as a potential therapeutic
target. However, previous studies in human cancer cells have
indicated that disrupting telomerase as a means of halting cancer
cell replication or inducing cell suicide would require an almost
complete loss of normal telomerase activity. And this would
require either swamping the enzyme with an overwhelming amount of
mutant telomerase or finding a sufficiently potent drug to
completely inhibit the enzyme.
But in the current study, the researchers observed that
inserting a tiny mutation in the gene coding for a small but
critical portion of the telomerase enzyme prompted a dramatic
response from cancer cells. The finding suggests a more efficient
means of delivering therapy. Most of the human breast and prostate
cancer cells grown in culture lost the ability to replicate or
they committed suicide, while tumors formed from human breast
cancer cells grafted into mice were smaller than those generated
from cells that didn't have the mutation. Moreover the response
occurred despite the fact that most of the normal telomerase was
retained. The researchers induced the response with several
different variations of the mutant gene.
