Stromal p16 expression is significantly increased in endometrial carcinoma
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Gun Yoon1,*, Chang Won Koh2,*, Nara Yoon3, Ji-Ye Kim4, Hyun-Soo Kim4
1Shinsegae Women’s Hospital, Daegu, Republic of Korea
2Department of Obstetrics and Gynecology, Seoul National University Hospital, Seoul, Republic of Korea
3Department of Pathology, The Catholic University of Korea Incheon St. Mary’s Hospital, Incheon, Republic of Korea
4Department of Pathology, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea
*These authors have contributed equally to this work
Hyun-Soo Kim, email: firstname.lastname@example.org
Keywords: p16, endometrium, peritumoral stroma, endometrioid carcinoma, serous carcinoma
Received: October 07, 2016 Accepted: November 16, 2016 Published: November 25, 2016
p16 is a negative regulator of cell proliferation and is considered a tumor suppressor protein. Alterations in p16 protein expression are associated with tumor development and progression. However, the p16 expression status in the peritumoral stroma has not been investigated in the endometrium. Therefore, we evaluated stromal p16 expression in different types of endometrial lesions using immunohistochemistry. Differences in the p16 expression status according to the degree of malignancy and histological type were analyzed. This study included 62, 26, and 36 cases of benign, precancerous, and malignant endometrial lesions, respectively. Most benign lesions showed negative or weak expression, whereas precancerous lesions showed a variable degree of staining proportion and intensity. Atypical hyperplasia/endometrial intraepithelial neoplasia (AH/EIN) and serous endometrial intraepithelial carcinoma (SEIC) had significantly higher stromal p16 expression levels than benign lesions. Endometrioid carcinoma (EC), serous carcinoma (SC), and carcinosarcoma showed significantly elevated stromal p16 expression levels compared with benign and precancerous lesions. In addition, there were significant differences in stromal p16 expression between AH/EIN and SEIC and between EC and SC. In contrast, differences in stromal p16 expression among nonpathological endometrium, atrophic endometrium, endometrial polyp, and hyperplasia without atypia were not statistically significant. Our observations suggest that stromal p16 expression is involved in the development and progression of endometrial carcinoma, and raise the possibility that p16 overexpression in the peritumoral stroma is associated with aggressive oncogenic behavior of endometrial SC.
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