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Imagine there’s an art museum, and the guard on
duty keeps dozing off. Art thieves come in. They step over the guard,
who is now snoring, and steal a valuable painting. The guard had
a gun, an alarm, and other anti-theft devices at his disposal, but
never used them. All that untapped firepower was wasted.
In our bodies, certain white blood cells called lymphocytes
are a lot like that guard. They have a great ability to attack and
destroy enemies, including bacteria and cancer cells. But when the
enemy is prostate cancer, for some reason, these lymphocytes — designed
to destroy these cancer cells — don’t do their job.
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White blood cells called
lymphocytes
have a great ability to attack
and destroy enemies. But when
the enemy is prostate cancer, for
some reason, they don’t work.
Oncologist Charles Drake,
M.D., Ph.D., the Phyllis and Brian L. Harvey Scholar, has figured
out why. “Using a mouse model, we found a protein on the surface
of some of these cells that might help explain this lack of function,” he
says. This protein is called LAG-3, and “by blocking it, we
were able to help lymphocytes move into prostate glands.” Basically,
Drake and colleagues put the sleeping soldiers back into action,
so they could help fight off prostate cancer. In other experiments,
they combined LAG-3- blocking with a specific vaccine against prostate
cancer, and this also jump-started the immune system, “causing
lymphocytes to move into the prostate gland and destroy their target
cells.” This work was published in the Journal
of Clinical Investigation. Drake hopes to test this strategy in men with prostate
cancer, “but first, we need to make a human version of the
LAG-3 blocking agent,” called a monoclonal antibody. He and
colleagues have teamed up with a leading biotechnology company to
do this. |
