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Blood-vessel blocker aids cancer-killing virus
Date:11/27/2007

s also triggered a twofold or greater change in the activity of 48 of 84 genes that are involved in inflammation and immune responses. Of those genes that were highly changed was the gene for interferon-gamma (IFNg), a substance important for coordinating immune responses to viral infections.

Together, these findings indicate that the oncolytic virus triggered a local immune response in the tumor that would curtail its effectiveness, Kaur says.

In other rats, the researchers injected into developing tumors an agent that blocks blood-vessel growth. Four days after that, they injected the virus into the tumors. The agent is called cRGD (cyclic peptide of arginine-glycine-aspartic).

Tumors in animals that received the agent had significantly fewer blood vessels than control animals (28 vs. 62 per area of tumor), and the vessels were significantly less leaky. Also, fewer immune cells were drawn to the tumor from the bloodstream.

Furthermore, the treated animals showed a more than twofold drop in the activity of 19 genes associated with inflammation, including the gene for IFNg.

Finally, animals pretreated with the blood-vessel-growth inhibitor lived an average of 21 days, while control animals that received only the virus lived 17 days.

The agent increased survival by about 23 percent, Kaur says, which means a lot because these tumors are very aggressive.


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Contact: Darrell E. Ward
darrell.ward@osumc.edu
614-293-3737
Ohio State University
Source:Eurekalert

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