Demonstration of focal p53 expression without genetic alterations in endometriotic lesions

Their monoclonal origin las indicated by recent investigations) indicates t he neoplastic nature of most endometriotic lesions, p53, a representative t umor suppressor, regulates cell proliferation, and genetic alterations in p 53 are involved in carcinogenesis in a wide variety of human cancers. The a im of this study was to examine endometriotic lesions for p53 expression an d genetic alterations in p53. An immunohistochemical study revealed that 20 % (13/64) of endometriotic lesions showed focal p53 expression in the epith elial cells. Using serial paraffin sections, we employed a microdissection method to extract DNA from the endometriotic tissues that showed p53 expres sion. No mutations were found in exons 5-8 in p53 by cleavase fragment leng th polymorphism scanning and polymerase chain reaction-DNA sequencing. More over, neither loss of heterozygosity nor microsatellite instability was det ected at the microsatellite marker sites of p53. These results suggest that the focal p53 expression recognized in the endometriotic epithelia may be due to overproduction of wild-type p53 protein.