Demonstration of focal p53 expression without genetic alterations in endometriotic lesions

Their monoclonal origin (as indicated by recent investigations) indicates the neoplastic nature of most endometriotic lesions. p53, a representative tumor suppressor, regulates cell proliferation, and genetic alterations in p53 are involved in carcinogenesis in a wide variety of human cancers. The aim of this study was to examine endometriotic lesions for p53 expression and genetic alterations in p53. An immunohistochemical study revealed that 20% (13/64) of endometriotic lesions showed focal p53 expression in the epithelial cells. Using serial paraffin sections, we employed a microdissection method to extract DNA from the endometriotic tissues that showed p53 expression. No mutations were found in exons 5-8 in p53 by cleavase fragment length polymorphism scanning and polymerase chain reaction-DNA sequencing. Moreover, neither loss of heterozygosity nor microsatellite instability was detected 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.