Mutant P53 In Tumor Cells Selectively Depleted By Chemopreventive Isothiocyanates

Researchers at Lombardi Comprehensive Cancer Center at Georgetown University Medical Center have demonstrated that naturally-occurring compounds can selectively deplete mutant p53 and restore “wild type” function to p53 in a variety of tumor cells. Mutations in the p53 tumor suppressor gene - which is involved in apoptosis and DNA repair - occur in about half of all human tumors. p53 often acts as a checkpoint preventing abnormal cells from continuing to grow and divide.

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