Critical innovations and new knowledge are now emerging from the laboratories of universities, medical centers and pharmaceutical companies worldwide, offering the prospect of a new generation of drugs capable of destroying cancer cells with pinpoint accuracy, without damaging adjacent normal cells.

Each year, the American Association for Cancer Research (AACR), jointly with the National Cancer Institute (NCI) and the European Organisation for Research and Treatment of Cancer (EORTC), brings together scientists and other professionals from around the world seeking to share the latest information in this field, otherwise known as molecular targets of cancer.

More than 2,500 scientists and clinicians including top executives and researchers from more than 300 pharmaceutical and biotech companies are gathering in Boston next week at the annual AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics to present, discuss and hear about such promising discoveries as:

• The Circadian Rhythm of Cells, in which the "clock genes" that coordinate many fundamental cell functions operate according to a diurnal schedule. Researchers have hypothesized that cancer often occurs when the timing of circadian clock genes is "off," resulting in an imbalance between cell proliferation and cell death. They believe these genes and their products represent novel targets for the control of cancer growth.
• Turning Tumors Against Themselves, by transforming the vascular endothelial growth factor (VEGF) from a promoter of angiogenic growth and survival to a cancer killer. One study shows that binding VEGF to the Fas apoptosis receptor, creating VEGFR2Fas, triggers the signal for cell death. Further investigation will seek to optimize this effect and determine the feasibility of using it in vivo to kill tumor cells and/or the blood vessels that fuel them directly.
• Improving the Effectiveness of Radiotherapy for som
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Contact: Warren Froelich
froelich@aacr.org
215-440-9300
American Association for Cancer Research
11-Nov-2003


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