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Tumor cells made more sensitive to radiation by blocking a key cellular molecule

breaking down another molecule, IkappaB. This molecule is attached to NF-kappaB and blocks it from activating. Much like a car's brakes, IkappaB stops NF-kappaB from moving into the nucleus, the cell's master control room.

The researchers also studied the effects of infusing tumor cells with a type of IkappaB that is a super-repressor of NF-kappaB. This super-repressor molecule when ferried into tumor cells via an inactivated cold virus creates a very stable attachment to NF-kappaB.

"We were able to determine that NF-kappaB inhibition by either method did in fact produce increased cell killing after radiation," Tepper said. "And we could document both increased cell killing and increased apoptosis."

Moreover, both Tepper and Russo point out that they also documented a decrease in "clonogenic survival." After treatment, tumor cells eventually ceased to divide and died. "This is the most important endpoint," Tepper said.

"We found that treatment with IkappaB super-repressor or PS-341 increased the radiation response," Russo said. "And when we went in vivo to look at mouse models and did the same interventions with tumors we grew on mice, we found the same thing.

"Potentially, agents that modify programmed cell death are exciting in that they may enhance the effects of our current anti-tumor therapies. As demonstrated by this study, radiation may work better in the presence of one of these agents."


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Contact: Leslie H. Lang
LLANG@MED.UNC.EDU
919-843-9687
University of North Carolina School of Medicine
24-Oct-2000


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