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New anti-inflammatory strategy for cancer therapy identified by UCSD researchers

imuli into tumor growth signals, it is also known to activate TNFα, a major proinflammatory protein initially thought to play a role in the death of cancer cells. Investigators first reasoned that TNFα might be responsible for the death of cancer cells in which NF-kB was inhibited, seen in this study, since previous experiments have shown that high doses of TNFα can kill tumor cells when NF-kB activity is inhibited.

However, further experiments proved otherwise. When inflammation-inducing LPS was administered to tumor-bearing mice with normal NF-kB, the result was a rapid and robust induction of circulating TNFα and eventual acceleration of cancer growth. However, administration of an anti-TNFα antibody five minutes after LPS challenge neutralized most of the circulating TNFα, inhibited NF-kB activation in cancer cells, and prevented the inflammation-induced acceleration of tumor growth.

Rather than TNFα, the team found that TRAIL, a member of the TNF superfamily and a relative of TNFα, was the specific protein responsible for the tumor death response. While both NF-kB and TRAIL are activated in response to inflammation, NF-kB takes control, inhibits cell death and promotes cancer growth. When NF-kB or TNFα were inhibited, however, TRAIL was able to strongly assert its ability to reduce tumor growth by killing cancer cells. The role of TRAIL was further illustrated in additional experiments where a neutralizing anti-TRAIL antibody was injected into the mice following the LPS challenge. The result was tumor growth.

In their summary, the researchers said that since TNFα does not make a major contribution to tumor killing and instead may promote tumor growth, it may be advisable to develop drugs which reduce inflammation-associated toxicities, block inflammation-induced tumor growth and clear the way for TRAIL to in
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Contact: Sue Pondrom
spondrom@ucsd.edu
619-543-6163
University of California - San Diego
20-Sep-2004


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