Re-Empowering P53

Drug Restores Cell Suicide in HPV-Related Head and Neck Cancer

Quintin PanResearchers have designed a drug to block a newly discovered mechanism by which the human papillomavirus (HPV) causes head and neck cancer. Though more study is needed, they believe the new agent might offer a safer treatment for these tumors when combined with a tapered dose of standard chemotherapy.

HPV-positive head and neck cancer has become three times more common since the 1970s, and it could reach epidemic levels in the future, say researchers at the OSUCCC – James who led the study.

“We believe these findings will help meet the real need for more effective and safer therapy for a growing number of HPV-positive head and neck cancer patients,” says principal investigator Quintin Pan, PhD, associate professor of Otolaryngology at Ohio State and a member of the Experimental Therapeutics Program at the OSUCCC – James.

The research, which mainly used head and neck cancer cells, shows that a protein produced by the virus blocks a protein made by the host cell. The cell protein, called p300, regulates a gene called p53 that both controls cell division and protects the body against cancer by causing cells to die before they become malignant.

By blocking the cell protein, HPV forces the host cell to live instead of die and to proliferate and form tumors. The prospective new drug, called CH1iB, prevents the viral protein from binding with the cell protein. This restores the function of the p53 tumor-suppressor gene and triggers the death of the cancer cells.

“Our study revealed a new mechanism for p53 inactivation in HPV-positive head and neck cancer, and this allowed us to develop an agent that disrupts that interaction and reactivates p53 in this disease,” Pan says. “Our preclinical studies show CH1iB can reactivate p53 and eliminate HPV-positive head and neck cancer cells.”

Published in the journal Oncogene.

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