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University of Pittsburgh receives $10 million grant for head and neck cancer

ine that targets the tumor-suppressing gene p53. A critical gene involved in the development of many cancers, p53 is damaged in most cancers and this damage is correlated with worse clinical outcomes. Previous research has indicated that mutant p53 also expresses non-mutant p53 peptides in tumors. When combined with dendritic cells, these p53 peptides may induce an immune response, decreasing the chance of cancer recurrence and the formation of secondary tumors.

In a final project, Jill Siegfried, Ph.D., professor of pharmacology, and Dr. Grandis will examine multiple signaling pathways implicated in the proliferation of head and neck cancer.

"Unfortunately, head and neck cancer tumors are challenging to treat because they develop strategies to escape the anti-tumor effects of most therapies," said Dr. Siegfried. "One way to address this difficulty is to develop therapeutic approaches that target multiple signaling pathways."

Drs. Siegfried and Grandis are examining the interaction of two types of protein receptors implicated in the proliferation of head and neck cancer, epidermal growth factor receptor (EGFR) and members of the G-protein-coupled receptor (GPCR) family. While both types are over-expressed in head and neck cancer, preliminary studies suggest that combining strategies that block both receptor families has a synergistic effect on inhibiting the growth of head and neck cancer cells.

With 36,200 estimated new cases and 11,000 deaths in 2003, head and neck cancer accounts for 4 percent to 5 percent of all newly diagnosed cancers in the United States. More than two-thirds of head and neck cancer patients have a locally advanced stage when diagnosed, which has a poor five-year survival even after treatment.


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26-Aug-2004


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