P53 IMMUNOHISTOCHEMISTRY OF ODONTOGENIC KERATOCYSTS IN RELATION TO RECURRENCE, BASAL-CELL BUDDING AND BASAL-CELL NEVUS SYNDROME

Mutation of the p53 tumour suppressor gene can produce a more stable p rotein that does not inhibit mitosis, accumulates in the nucleus and c an then be detected immunohistochemically in many human tumours using antibody CM-1. The protein has also been detected in odontogenic kerat ocysts. Routinely processed material from 30 odontogenic keratocysts w as immunostained with antibody CM-1. Ten were recurrences and five wer e associated with the basal-cell naevus syndrome (Gorlin-Goltz syndrom e). p53 protein was found in 50% (15/30) of the odontogenic keratocyst s, in 53.3% (8/15) of non-recurrent cysts, in 40% (4/10) of recurrent cysts and in 60% (3/5) of those associated with the basal-cell naevus syndrome. Staining was weak and speckled and limited to occasional bas al and suprabasal cells. There was no statistically significant differ ence in staining between these groups and no correlation between expre ssion and the presence of satellite cysts, basal-cell budding or islan ds of odontogenic epithelium. The low levels of expression may represe nt physiological expression of wild-type p53 protein rather than mutan t or complexed p53 protein.