Uterine leiomyosarcoma (ULMS) with osteoclast-like giant cells (OLGCs) has been reported as a rare phenomenon in ULMS, and its clinico-pathological features and tumorigenesis remain unclear. We recently reported high expression of receptor activator of nuclear factor κB ligand (RANKL) in ULMS with OLGCs. As osteoblasts produce RANKL, in this study, we analyzed the expression of Runt-related transcription factor 2 (RUNX2), a critical transcription factor for osteoblasts, and osteoclast-related proteins in three cases of ULMS with OLGCs as well as five conventional ULMSs and nine leiomyomas. Immunohistochemistry and real-time reverse transcription quantitative polymerase chain reaction analyses showed high expression of RUNX2 and RANKL in ULMS with OLGCs. In these cases, macrophages expressed receptor activator of nuclear factor κB (RANK), and OLGCs expressed osteoclast-related proteins (nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), and cathepsin K). Accumulation sites of cathepsin K–positive OLGCs showed hemorrhagic appearance and degraded type IV collagen. We reviewed reported cases of ULMS with OLGCs, including ours, and found that they presented an aggressive course even at stage I. Furthermore, metastatic lesions showed similar histological features to those of OLGC association in ULMS. Here, we show that tumor cells in ULMS with OLGCs highly express RUNX2 and RANKL and that osteoclastic differentiation of macrophages occurs in the tumor tissue.

子宫平滑肌肉瘤（ULMS）和破骨细胞样巨细胞（OLGCs）已被报道是ULMS中的一种罕见现象，其临床病理特征和肿瘤发生机制尚不清楚。我们最近报道了ULMS和OLGC中核因子κB配体（RANKL）受体激活剂的高表达。由于成骨细胞产生RANKL，在本研究中，我们分析了3例带有OLGC的ULMS和5例常规ULMS中，与成骨细胞的关键转录因子Runt相关转录因子2（RUNX2）和破骨细胞相关蛋白的表达。九个平滑肌瘤。免疫组织化学和实时逆转录定量聚合酶链反应分析显示，RUNMS2和RANKL在带有OLGC的ULMS中高表达。在这些情况下，巨噬细胞表达了核因子κB（RANK）的受体激活剂，OLGCs表达破骨细胞相关蛋白（活化T细胞，细胞质1（NFATc1）和组织蛋白酶K的核因子）。组织蛋白酶K阳性OLGC的积累部位表现出出血现象和IV型胶原降解。我们审查了包括我们在内的报告的ULMS与OLGC的病例，发现它们甚至在I期也表现出侵袭性病程。此外，转移性病变的组织学特征与ULMS中的OLGC关联相似。在这里，我们显示具有OLGC的ULMS中的肿瘤细胞高表达RUNX2和RANKL，并且巨噬细胞的破骨细胞分化发生在肿瘤组织中。组织蛋白酶K阳性OLGC的积累部位表现出出血现象和IV型胶原降解。我们回顾了包括OLGCs在内的ULMS与OLGC的报道病例，发现它们甚至在I期都表现出侵袭性病程。此外，转移性病变的组织学特征与ULMS的OLGC关联相似。在这里，我们显示具有OLGC的ULMS中的肿瘤细胞高表达RUNX2和RANKL，并且巨噬细胞的破骨细胞分化发生在肿瘤组织中。组织蛋白酶K阳性OLGC的积累部位表现出出血现象和IV型胶原降解。我们审查了包括我们在内的报告的ULMS与OLGC的病例，发现它们甚至在I期也表现出侵袭性病程。此外，转移性病变的组织学特征与ULMS中的OLGC关联相似。在这里，我们显示具有OLGC的ULMS中的肿瘤细胞高表达RUNX2和RANKL，并且巨噬细胞的破骨细胞分化发生在肿瘤组织中。