(Toronto, June 21, 1999) - The cellular fuel which powers the growth of Hodgkin's disease has been identified for the first time by a research team at Princess Margaret Hospital's Ontario Cancer Institute, the University of Toronto and the Amgen Research Institute. The research team also discovered that the fuel is actually manufactured by the tumour cells themselves.

The finding paves the way for future research into targeted ways to stop the growth of Hodgkin's disease tumours with little or no side effects, and is the cover article in the June 21, 1999 edition of the Journal of Experimental Medicine.

"Huge Clinical Potential"
"I'm particularly excited because for the first time we have identified the engine that drives at least some Hodgkin's cancer cells to multiply. We are now working to find a way to shut down that engine. These findings have huge clinical potential," said Dr. Tak W. Mak, senior scientist at the Ontario Cancer Institute, director of the Amgen Research Institute and professor of Medical Biophysics and Immunology at the University of Toronto.

Researchers discovered that a growth factor, called Interleukin-13 (IL-13), is secreted by Reed-Sternberg cells, the cancer cells of Hodgkin's disease. IL-13 then fuels the growth of more Reed-Sternberg cells in a cyclical process of self-proliferation.

Using gene chip technology, lead author Dr. Ursula Kapp, a scientist at the Amgen Institute at the time of the study and now a member of the departments of hematology and oncology at University Medical Centre in Freiburg, Germany, examined 950 tumour genes in order to identify which ones are specifically expressed in Hodgkin's disease cells. She found that IL-13 is consistently over-expressed in Hodgkin's disease. Her colleague, Dr. Bruce Patterson, a pathologist at Princess Margaret Hospital and co-author of the study, determined that it was the Reed-Sternberg cells themselves that produce the deadly growth factor.

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Contact: Steven de Sousa
stven.desousa@utoronto.ca
416-978-5949
University of Toronto
21-Jun-1999