A new strategy for cancer therapy, which converts the tumor-promoting effect of the immune system's inflammatory response into a cancer-killing outcome, is suggested in research findings by investigators at the University of California, San Diego (UCSD) School of Medicine.

The findings provide new insight into the immune system's response to inflammation, the connection between inflammation and malignancy, and how the delicate balance between cancer promotion and inhibition can be manipulated in the patient's favor, according to the study's senior author, Michael Karin, Ph.D., UCSD professor of pharmacology, American Cancer Society Research Professor, and a member of the Rebecca and John Moores UCSD Cancer Center.

The studies in mice with colon or breast cancer showed that cancer metastasis, the growth of malignant tumors beyond the original site, was halted with inhibition of either one of two naturally occurring substances, a pro-inflammatory protein called nuclear factor-kappa B (NF-kB) or an inflammatory mediator called tumor necrosis factor alpha (TNFa).

The result, published in the journal Cancer Cell, was increased effectiveness of a cancer-killing protein called TNF-related apoptosis-inducing ligand (TRAIL), leading to a decrease in cancer cells and increase in the life span of tumor-bearing mice.

SOURCES:
Cancer Cell, September 20, 2004
University of California, San Diego (http://www.ucsd.edu)