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Significance of Beta-Catenin Expression for the Incidence of Pathological Fractures in Giant Cell Tumors of Bone

Authors :
Sopta, Jelena
Lujić, Nenad
Kovačević, Relja
Davidović, Radoslav S.
Sopta, Jelena
Lujić, Nenad
Kovačević, Relja
Davidović, Radoslav S.
Source :
Polish Journal of Pathology
Publication Year :
2016

Abstract

Aim of the study is to determine the possible roles of p53, cyclin D1, B-catenin and Ki-67 in the increase in risk of fractures in patients with giant cell tumor of bone. The study included a total of 164 patients with giant cell tumor of bone (GCTB), 21 (12.8%) with and 143 (87.2%) without fracture. The samples were analyzed immunohistochemically for expression of Ki-67, p53, cyclin D1 and beta-catenin. According to the immunohistochemical expression of p53 and Ki-67 in mononuclear stromal cells, as well as of cyclin D1 in multinuclear giant cells, there was no significant association with immunopositivity and risk of fractures. However, our research revealed that patients with cytoplasmic expression of beta-catenin in stromal cells had three times more frequent occurrence of pathological fractures, which was highly statistically significant (chi(2) = 7.065; p = 0.008). Moreover, a highly statistically significant correlation between the nuclear expression of beta-catenin in giant cells and the incidence of pathological fractures was also found (chi(2) = 8.824; p = 0.003). The study showed that beta-catenin expression highly correlates with the incidence of pathological fractures in patients with GCTB. Taking into account that beta-catenin is closely linked to activation of the Wnt signaling pathway in GCTB pathogenesis, one could postulate that activation of the Wnt pathway is one of the contributing factors to locally destructive behavior of this tumor, as well as to the incidence of pathological fractures.

Details

Database :
OAIster
Journal :
Polish Journal of Pathology
Notes :
Polish Journal of Pathology
Publication Type :
Electronic Resource
Accession number :
edsoai.on1085020022
Document Type :
Electronic Resource