Ovarian cancer arises from the accumulation of mutations in multiple combinations of genes (1 ). The most extensively studied tumor suppressor gene in solid tumors isp53,a 53-kD nuclear phosphoprotein that binds DNA. Thep53gene product plays a role in normal cellular proliferation by regulating gene transcription, cell cycle control, and apoptosis (2 ). Mutations ofp53are the most common molecular genetic abnormality to be described in human cancer, and have been identified in malignancies of the breast, colon, lung, esophagus, head and neck, and hematopoietic system (3 ). Mutations of thep53gene have been identified in 30 to 79% of epithelial ovarian cancers (4 ,5 ). Most of the mutations identifiedin p53are distributed throughout the open reading frame as missense mutations. We have identified a missense mutation in thep53gene in the 2774 ovarian cancer cell line that converts an arginine residue in the DNA binding region of the protein to a histidine residue (6 ). The mutation in codon 273 we found in 2774 cells is one of the six major hotspots identified forp53missense mutations (7 ).
