Demonstration of focal p53 expression without genetic alterations in endometriotic lesions

Nakayama K, K Nakayama, T Toki, Toki T, Zhai YL, Y L Zhai, X Lu, Lu X, A Horiuchi, Horiuchi A, T Nikaido, Nikaido T, Konishi I, I Konishi, S Fujii, Fujii S
International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2001 · doi:10.1097/00004347-200107000-00004 · PMID:11444197
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This study found focal p53 expression in endometriotic lesions without detecting genetic alterations in the p53 gene, suggesting overproduction of wild-type p53 protein.

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This study investigated the presence of p53 protein expression and associated genetic alterations within endometriotic lesions to better understand their neoplastic nature. Researchers analyzed 64 samples using immunohistochemistry and found focal p53 expression in 20% of cases, but subsequent DNA sequencing and microsatellite analysis revealed no mutations or loss of heterozygosity in the p53 gene. The authors concluded that the observed protein accumulation likely results from the overproduction of wild-type p53 rather than genetic dysfunction. This paper is centrally about endometriosis — specifically examining molecular markers like p53 in endometriotic epithelial cells.

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Abstract

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.
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Demonstration of Focal p53 Expression without Genetic Alterations in Endometriotic Lesions - Kuniaki Nakayama - Toshihiko Toki - Ya-Li Zhai - Xin Lu - Akiko Horiuchi - Toshio Nikaido - Ikuo Konishi - Shingo Fujii Summary: 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.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Genes, p53 Adult Aged DNA Mutational Analysis Endometriosis Endometriosis Endometriosis Female Humans Immunohistochemistry Microsatellite Repeats Middle Aged Mutation Tumor Suppressor Protein p53 Tumor Suppressor Protein p53

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