before it's in the papers"
August 03, 2010
TO THE WORLD SCIENCE HOME PAGE
Engineered virus makes cancer cells “eat themselves”
and World Science staff
Researchers say they have engineered a virus that tracks down cancerous cells and forces them to devour themselves.
The scientists, with the University of Texas M. D. Anderson Cancer Center, tested the treatment in mice with brain tumors, and described the results this week in the Journal of the National Cancer Institute.
The virus induced self-cannibalization among cancer cells, a process called autophagy, thus shrinking tumors and extending survival, said the center’s Seiji Kondo. His team of researchers developed the treatment by modifying an adenovirus, one of a group of viruses that cause the common cold and various other infections.
Among mice with brain tumors known as gliomas, those treated with three injections of the modified virus on average lived 53 days, the researchers said. Those that received a different, non-replicating adenovirus lived on average 29 days.
Gliomas are the most common and deadly form of brain cancer, the researchers said.
‘‘This virus uses telomerase, an enzyme found in 80 percent of brain tumors, as a target,’’ Kondo said. ‘‘Once the virus enters the cell, it needs telomerase to replicate. Normal brain tissue does not have telomerase, so this virus replicates only in cancer cells.’’
Other cancers are also associated with telomerase, the researchers said, adding that they found in lab experiments that the treatment may also work with prostate and cervical cancer.
Besides showing the therapeutic potential of the virus, called hTERT-Ad, Kondo said his international research team also clarified how the modified viruses works.
Autophagy is a natural, protective process that cells employ to consume part of themselves when nutrients are scarce, or to recycle their own worn-out components. A membrane forms around the material to be consumed, then everything inside is digested.
Kondo and colleagues found that hTERT-Ad induced autophagy by inactivating a molecular pathway that is known to prevent cellular self-cannibalization.
The pathway is distinct from apoptosis, a much better known process of programmed cellular “suicide.” A normal defense mechanism to systematically kill defective cells, apoptosis is dysfunctional in cancer cells. Many other cancer therapies focus on restoring or enhancing apoptosis to combat the disease.
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