The Role of p53 Mutation in the Carcinomas Arising from Endometriosis

Abstract

To probe the mechanism of the development of ovarian cancer from endometriosis, which is a multistep process that involves the activation of oncogenes and inactivation of tumor suppressor genes, we evaluated p53 mutations in solitary endometriosis and endometriosis coexisting with ovarian clear cell carcinoma (OCCA) and ovarian endometrioid carcinoma (OEC). We examined 7 cases of solitary ovarian endometriosis, 13 cases of OCCA, and 9 cases of OEC. Cancer tissue specimens that also contained endometriosis without atypia were chosen. Using a laser microdissection system, epithelial cells from the areas of endometriosis were isolated, and DNA was extracted. We amplified exons 5, 6, 7, and 8 of the p53 gene, and direct sequencing was performed. p53 mutation was observed in 4 (30.8%) of 13 specimens of endometriosis coexisting with OCCA, whereas no mutations were detected in solitary endometriosis or endometriosis coexisting with OEC. We thought that some genetic alterations, which induce p53 mutations in endometriosis, may affect malignant transformation of endometriosis into OCCA.

Association of TP53 gene codon 72 polymorphism with endometriosis in Mexican women

“…Ghasemi et al (2010) reported that Iranian women with the proline allele of TP53 codon 72 polymorphism had an increased risk of endometriosis cancer. Akahane et al (2007) found mutations in the TP53 gene of 30.8% (4/13) of endometrial tissues coexisting with ovarian clear cell carcinoma, and Kang et al (2009) suggested that proline allele of codon 72 polymorphism of TP53 regulates the efficiency of human reproduction.…”

Abdominopelvic Complications of Endometriosis

“…Other locations include: bowel, umbilicus, lymph node, urinary tract, pleura, diaphragm, lung, etc (Slavin et al, 2000;Van Gorp et al, 2004;Yantiss et al, 2001). Two possible explanations for the relation-ship between endometriosis and intraperitoneal cancer have been proposed: (i) endometriotic implants undergo malignant transformation secondary to genetic defects (p53 mutations) (Akahane et al, 2007) that also serve to enable the endometriosis to thrive, or (ii) women with endometriosis have a defect in their immune system that enables the endometriosis to flourish, and this baseline defect leaves them more susceptible to subsequent malignant transformation (Modesitt et al, 2002). It has been seen a direct transition from clearly benign epithelium through atypical endometriosis to carcinoma.…”

Current Insights and Future Advances in Endometriosis Diagnostics

“…The altered tumour suppressor genes might be related with the development of endometriosis. p53, a representative tumour suppressor, is involved in cell proliferation and progression of various tumour types (Akahane et al, 2007).…”