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Preventing cancer: Scientists identify a useful piece of JNK

A team of scientists led by Dr Roger Davis has discovered that a group of genes encoding the so-called 'JNK signaling pathway' can function to suppress tumor development by promoting tumor cell death. This finding, published in the March 1st issue of G&D, is particularly exciting since previous studies suggested that this pathway was important in promoting tumor growth. These new experiments have significant implications for the diagnosis and treatment of some forms of cancer.

The JNK signaling pathway allows cells to respond to changes in their extracellular environment and in doing so, controls many aspects of cell function including cell proliferation, differentiation and death. Studies have also shown that this pathway plays a role in cancer, although it has been unclear whether active JNK signaling can accelerate or protect cells from becoming cancerous. Several studies using cultured cells have suggested that JNK signaling may be important for promoting tumor cell development, while studies of tumors from human patients have indicated that JNK signaling may act to suppress tumor development.

Dr. Davis and colleagues set out to address the role of JNK signaling in tumor formation using cells from mice that have been engineered to be deficient in JNK signaling. They demonstrated that in vitro, JNK signaling does indeed play a role in transforming normal cells into those displaying the characteristics of tumor cells.

However, when they moved their experiments into a mouse model of tumor development, it was clear that JNK signaling is not required for tumor formation. In fact, the scientists actually found the opposite - that the absence of JNK signaling resulted in a dramatic increase in the number and growth of tumors when compared to control animals. This result suggests that in vivo, JNK signaling acts to suppress tumor development.

The scientists went on to examine how JNK signaling puts the brakes on tumor development and pr
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Contact: Michele McDonough
mcdonoug@cshl.org
Cold Spring Harbor Laboratory
5-Mar-2003


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