This discovery, reported in the June 24 on-line issue of Nature Cell Biology, could provide scientists with a promising new target for the development of a drug to halt tumor invasion and metastasis, the spread of cancer from its primary site to other areas of the body.

Metastasis occurs when cancer cells penetrate the boundaries of the tumor's tissue and infiltrate the walls of blood vessels or lymph vessels, gaining a means of transport to other parts of the body far from the original tumor site where they can then grow anew. This process is unique to cancer cells and is what makes the disease so dangerous and so feared.

"A primary [cancerous] tumor can be removed," explains the study's senior author Alex Toker, Ph.D., of the department of pathology at Beth Israel Deaconess Medical Center (BIDMC) and assistant professor at Harvard Medical School. "But once the cancer has metastasized, it becomes intractable." In fact, the goal of early cancer detection is to remove the primary carcinoma before it has a chance to spread.

Scientists have known that in order for a tumor to metastasize, certain genes had to be "turned on" so that they could produce enzymes necessary to invade blood vessel walls and penetrate other tissues. Toker and his coauthors at BIDMC and at the Center for Blood Research at Harvard Medical School, set out to identify how this was happening, and began by focusing on the actions of a group of proteins known as transcription factors, including NFAT (nuclear factor of activated T cells).

NFAT, which is critical for efficient immune cell responses, was first identified in the cells of the immune system about 20 years ago. It subsequently became the target for cyclospo
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Contact: Bonnie Prescott
bprescot@caregroup.harvard.edu
617-667-7306
Beth Israel Deaconess Medical Center
24-Jun-2002