Giant Cell Tumor of the Tendon Sheaths of the Fingers

Abstract

Giant cell tumor of bone (GCTB) is a benign neoplasm but occasionally shows local recurrence, and histologically consists of osteoclast-like giant cells (GC) and stromal mononuclear cells (SC), which are capable of proliferation and osteoblastic differentiation. Activation of Wnt signaling can induce osteoblast differentiation and osteoclastgenesis during bone resorption process. This study analyzed the profiles of β-catenin and cyclin D1 expression in GCTB to elucidate an involvement of Wnt pathway in tumorigenesis. We performed immunohistochemistry for β-catenin, cyclin D1, and Ki-67 in 16 GCTB tumors, including 5 recurrent cases that were surgically resected. All 16 cases of GCTB displayed β-catenin, cyclin D1, and Ki-67 expression. Immunoreactivity for β-catenin was observed in nuclei of SC and GC. Cyclin D1 immunoreactivity was found mainly in nuclei of GC, while Ki-67 immunoreactivity was restricted to nuclei of SC. The nuclear β-catenin labeling index (LI) in both SC (60.6 vs. 41.8%, p=0.074) and GC (41.7 vs. 20.1%, p=0.095) was higher in recurrent tumors than in primary tumors in all the 4 cases. However, Ki-67 LI in SC (18.8 vs. 19.9%, p=0.851) and cyclin D1 LI in GC (55.4 vs. 70.1%, p=0.225) were not higher in recurrent tumors than in primary tumors. Our results suggested activation of Wnt/ β-catenin pathway in GCTB tumorigenesis. Since cyclin D1 in GC was never associated with the expression of the well-known proliferative marker Ki-67, cyclin D1 expression might play a role in GC formation instead of promoting cell proliferation during GCTB tumorigenesis. Importantly, it was suggested that the nuclear β-catenin staining level might be associated with tumor recurrence in GCTB.