Cold sore virus transformed into a better
cancer killer
NEW YORK -- July 13,
2001 (Cancer Digest) -- Scientists have found a way to boost
the cancer-killing ability of a genetically modified virus that
normally causes cold sores. The research could lead to more potent
anti-cancer therapies for prostate and other types of cancers.
New York University
School of Medicine researchers report in the July 17 print edition
of the Proceedings of the National Academy of Sciences that they
have isolated a new version of a herpesvirus that kills cancer
cells but spares normal tissue.
Dr. Ian Mohr, assistant
professor of microbiology at NYU, who led the research, cautions
that the study was done in mice, and no human studies using the
new virus have been attempted.
"We took a crippled
virus and essentially made it into a more effective killer of
cancer cells," he said in a prepared statement. "Clearly
the next step is to see whether this more potent anti-tumor virus
works in other animal models."
The NYU team injected
a new version of the genetically engineered herpesvirus with
an added mutation directly into human prostate cancer tumors
growing in specially bred mice that had no immune systems. In
another group of mice, they injected an earlier version of the
herpesvirus, and in the last group they injected an inert solution
that didn't contain virus.
Thirty-four days after
the treatment, the tumors injected with the new version were,
on average, eight times smaller than the tumors injected with
the older version of the virus. Moreover, the tumor mass had
completely disappeared in up to 40 percent of the animals injected
with the new version of the virus.
Dr. Samir Taneja, assistant
professor of urology, who is a co-author of the study says the
result represents a significant advance developing anti-cancer
viruses.
"We think this
new virus offers great promise as a therapeutic strategy for
the treatment of patients with prostate cancer," he says.
"Eventually we hope to test this virus in humans but we
still have many things to work out.".
While it has been more
than a decade since scientists learned how to create disarmed
viruses that target rapidly dividing cells, progress has been
stymied by an inability to infect all the cells in a tumor.
The result says Mohr,
"is that the virus doesn't completely destroy the tumor
mass, and the surviving cancer cells can simply grow."
To solve this problem,
Mohr's group observed the effect of the genetically engineered
herpesvirus on human cancer cells grown in a laboratory dish.
They isolated the viral strain that was the most effective killer
of cells and discovered that it contained an extra genetic mutation
that enabled more robust reproduction of the virus.
This extra mutation
switches the production of a protein called Us11 to an earlier
time in the infection cycle of the virus, which prevents the
cell from mounting a response to stop viral replication.
Although this kind
of viral research is still in its infancy at least 10 different
cancer-killing viruses are in early clinical trials or will be
soon.
SOURCE: Proc. Natl. Acad. Sci.
USA, www.pnas.org/cgi/doi/10.1073/pnas.161011798
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