Institutional members access full text with Ovid®

Share this article on:

Overexpression of p53 in the endometrial gland in postmenopausal women

Koi, Chiho MD1; Hachisuga, Toru MD1; Murakami, Midori MD1; Kurita, Tomoko MD1; Nguyen, Thuy Thi MD1; Shimajiri, Shohei MD2; Fujino, Yoshihisa MD3

doi: 10.1097/GME.0000000000000265
Original Articles

Objective The p53 signature, which (although morphologically unremarkable) displays diffuse and strong p53 nuclear staining, has been proposed to be a precursor of serous endometrial intraepithelial carcinoma. We examined the overexpression of p53 in postmenopausal endometrial glands.

Methods Postmenopausal endometrial tissues of 82 women with benign disease, including 10 hormone users, were evaluated in this study. Tissues with endometrial hyperplasia and/or polyps were excluded based on a histopathologic review. Expressions of estrogen receptor-α, Ki-67, and p53 were immunohistochemically examined. Apoptotic cells were identified using a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Overexpression of p53 was categorized as moderate to strong in more than 50% of glandular cell nuclei.

Results Focal glandular overexpression of p53 was observed in 1 (9%) of 10 and in 8 (11%) of 72 postmenopausal endometrial tissue specimens in women with and women without a history of hormone use, respectively. Among nonhormone users, the median Ki-67 and apoptotic indices in the postmenopausal endometrial glands of women with and women without overexpression of p53 were 16% and 6% (P = 0.007) and 1% and 1% (P = 0.345), respectively. All postmenopausal endometrial glands were positive for estrogen receptor-α, regardless of the overexpression of p53. The postmenopausal endometrial glands of estrogen users exhibited significantly higher Ki-67 and apoptotic indices than those of nonestrogen users (P = 0.001 and P < 0.001, respectively).

Conclusions Overexpression of p53 may be responsible for the high proliferative activity of postmenopausal endometrial glandular cells associated with conditions of low apoptotic cell death.

From the Departments of 1Obstetrics and Gynecology, 2Pathology and Cell Biology, and 3Preventive Medicine and Community Health, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishi-ku, Kitakyushu, Japan.

Received January 16, 2014; revised and accepted March 27, 2014.

Funding/support: None.

Financial disclosure/conflicts of interest: None reported.

Address correspondence to: Toru Hachisuga, MD, Department of Obstetrics and Gynecology, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan. E-mail:

© 2015 by The North American Menopause Society.