Alternative Title子宮内膜症性嚢胞の悪性転化におけるHO-1発現マクロファージの特徴
Periodical titlePathology, research and practice
Note (General)type:Thesis
Malignant transformation of endometriosis is a rare and still poorly understood event, but is associated with the distortion of the pro-oxidant and anti-oxidant balance. The aim of the present study was to quantify the numbers of macrophages polarized as M1 or M2 phenotypes and the expression of heme oxygenase (HO)-1 in tissue sections from patients with benign ovarian endometrioma (OE) and its malignant transformation (endometriosis-associated ovarian cancer, EAOC). We performed a retrospective study at the Department of Gynecology, Nara Medical University hospital from December 2012 to March 2015. This study included 53 patients with OE (n = 33) and EAOC (n = 20), and we evaluated polarized functional status of macrophages by immunohistochemical staining of CD68, CD11c, CD163 and HO-1. The number of the M1 phenotype (CD11c+, p = 0.001) and the M2 phenotype (CD163+, p = 0.009) was significantly lower in EAOC patients than in OE patients. Analyzing the correlations between the studied markers, the expression of CD68, CD11c, and CD163 proteins significantly correlated with each other (p < 0.001). The number of M2 phenotypes expressing HO-1 was significantly decreased in the EAOC group, compared with the OE group (P < 0.001), demonstrating sustained downregulation of an antioxidant marker, HO-1, in EAOC. In conclusion, reduced number of M2 macrophages expressing HO-1 may have an important role in promoting malignant transformation of OE.
博士(医学)・乙第1434号・令和元年9月27日
Copyright © 2018. Published by Elsevier GmbH.
identifier:Pathology, research and practice Vol.215 No.4 p.639-643 (2019 Apr)
identifier:03440338
identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3670
identifier:Pathology, research and practice, 215(4): 639-643
DOIinfo:doi/10.1016/j.prp.2018.12.017
Collection (particular)国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
Date Accepted (W3CDTF)2020-05-25T09:38:44+09:00
Data Provider (Database)国立国会図書館 : 国立国会図書館デジタルコレクション