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Page: << Prev | 1 | 2 | 3 | Next >> "T-cells are field marshals of the immune system," explained Dr. Thomas Kipps, of the Moores UCSD Cancer Center in La Jolla, Calif. "They direct traffic, recognize when foreign invaders come into the body, and they can induce formation of killer cells to go after the invader."
In this case, the drug induces the T-cells to attack cancerous cells, long a goal of cancer researchers.
"The antibody decorates tumor cells so any passing T-cell touching that cell briefly will adhere to it much longer than normal, and then the whole program of cell killing is kicked off," Baeuerle said.
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That approach is different from the one used by most antibody therapeutics, which flag diseased cells but do not necessarily recruit T-cells to kill them, Kipps said.
"I think it's exciting that we have new tools to treat cancer," Kipps said. "Whenever you have specificity to act against the cancer cell and also solicit host systems to combat the cancer, I think that's an advance."
"The promise of this technology is phenomenal," Kamen added.
That's because similar BiTE compounds, designed to target other kinds of cells, can easily be built by replacing the B-cell-targeting arm with one targeting, say, melanoma or breast cancer cells.
Baeuerle said Micromet has already developed and is testing other BiTEs against, for instance, EpCAM, a molecule that decorates a variety of solid tumors such as colon and lung cancers.
One potential drawback of blinatumomab, both Kamen and Kipps said, involves its mechanism of targeting B cells. Rather than homing in on diseased cells in particular, the drug targets all B cells. As a result, it leads to rapid depletion of B-cell pools.
"If I give this to a person with a normal immune system, will I take out all the B cells?" Kamen asked. "Probably, and you have to ask yourself what the significance of that is."
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