A team led by biochemists at the University of California, San Diego has found what could be a long-elusive mechanism through which inflammation can promote cancer. The findings may provide a new approach for developing cancer therapies.
The study, published in the January 26 issue of the journal Cell, shows that what scientists thought were two distinct processes in cells--the cells' normal development and the cells' response to dangers such as invading organisms--are actually linked. The researchers, who were also from the Salk Institute for Biological Studies and the La Jolla Institute for Allergy and Immunology, say that the linkage of these two processes may explain why cancer, which is normal growth and development gone awry, can result from chronic inflammation, which is an out-of-control response to danger.
"Although there is plenty of evidence that chronic inflammation can promote cancer, the cause of this relationship is not understood," said Alexander Hoffmann, an assistant professor of chemistry and biochemistry at U.C. San Diego, who led the study. "We have identified a basic cellular mechanism that we think may be linking chronic inflammation and cancer."
Cellular defense is a rapid process compared to cellular development, just as a state's response to terrorist threats is swifter than the construction of new infrastructure. However, in both settings, safeguarding against threats and building structures have certain steps in common and require similar types of workers, or molecules.
Hoffmann referred to the parallel sets of steps in cellular defense and development as "mirror image pathways." His team showed that these pathways are not distinct from one another because they are linked by a protein called p100. They found that inflammation leads to an increase in p100, but that p100 is also used in certain steps in development. Therefore p100 allows communication between inflammation and developm
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Contact: Sherry Seethaler
sseethaler@ucsd.edu
858-534-4656
University of California - San Diego
25-Jan-2007