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伴有破骨细胞样巨细胞的子宫平滑肌肉瘤与核因子κB受体激活剂配体的高表达相关

Uterine leiomyosarcoma with osteoclast-like giant cells associated with high expression of receptor activator of nuclear factor κB ligand.

作者信息

Terasaki Mika, Terasaki Yasuhiro, Yoneyama Koichi, Kuwahara Naomi, Wakamatsu Kyoko, Nagahama Kiyotaka, Kunugi Shinobu, Takeshita Toshiyuki, Shimizu Akira

机构信息

Department of Analytic Human Pathology, Nippon Medical School, Tokyo 113-8602, Japan.

Department of Analytic Human Pathology, Nippon Medical School, Tokyo 113-8602, Japan.

出版信息

Hum Pathol. 2015 Nov;46(11):1679-84. doi: 10.1016/j.humpath.2015.04.018. Epub 2015 Jul 21.

DOI:10.1016/j.humpath.2015.04.018
PMID:26315618
Abstract

The occurrence of osteoclast-like giant cells (OLGCs) in uterine leiomyosarcomas (LMSs) is a rare phenomenon. The nature of OLGCs and the significance of their accumulation in these tumors are poorly understood. Recent studies revealed that the formation of osteoclasts requires a specific cytokine, receptor activator of nuclear factor κB ligand (RANKL), in bone. In this study, we investigated the expression of RANKL in 2 cases of uterine LMS with OLGCs by means of immunohistochemistry and compared the extent of RANKL expression with that in conventional uterine LMSs and leiomyomas by using real-time reverse-transcription quantitative polymerase chain reaction. Our cases of uterine LMS with OLGCs showed markedly high expression of RANKL messenger RNA with clear RANKL immunoreactivity compared with messenger RNA expression and immunoreactivity of conventional uterine LMSs and leiomyomas. These findings suggest that the tumors producing RANKL may account for accumulation of OLGCs in tumor tissue because of RANKL-related osteoclastogenesis.

摘要

破骨细胞样巨细胞(OLGCs)出现在子宫平滑肌肉瘤(LMSs)中是一种罕见现象。OLGCs的本质及其在这些肿瘤中聚集的意义目前尚不清楚。最近的研究表明,破骨细胞的形成需要一种特定的细胞因子——骨中的核因子κB受体活化因子配体(RANKL)。在本研究中,我们通过免疫组织化学方法研究了2例伴有OLGCs的子宫LMS中RANKL的表达情况,并通过实时逆转录定量聚合酶链反应,将RANKL的表达程度与传统子宫LMS及平滑肌瘤进行比较。与传统子宫LMS及平滑肌瘤的信使核糖核酸表达和免疫反应性相比,我们的伴有OLGCs的子宫LMS病例显示出RANKL信使核糖核酸的显著高表达以及明显的RANKL免疫反应性。这些发现表明,产生RANKL的肿瘤可能是由于RANKL相关的破骨细胞生成,导致OLGCs在肿瘤组织中聚集。

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Virchows Arch. 2021 May;478(5):893-904. doi: 10.1007/s00428-020-02996-1. Epub 2021 Jan 6.