beta-Catenin is expressed aberrantly in tumors expressing shadow cells. Pilomatricoma, craniopharyngioma, and calcifying odontogenic cyst.
ABSTRACT We studied the beta-catenin immunohistochemical profile in tumors expressing shadow cells: pilomatricoma, 10 cases; calcifying odontogenic cyst, 6 cases; and craniopharyngioma, 9 cases. There was strong membranous, cytoplasmic, and nuclear staining of the immature basaloid cells in all of these tumors. Shadow cells were negative in all tumors. It has been documented that rising levels of free beta-catenin drive the formation of complexes with T-cell factor/lymphoid enhancer factor (TCF-Lef) and up-regulate the wingless-Wnt cell-cell signals. The end result is an abnormality of beta-catenin degradation and, thus, a buildup of free beta-catenin in the cytoplasm and/or nucleus, resulting in the stimulation of cellular proliferation and/or inhibition of cell death. beta-Catenin seems to have an important role in the oncogenesis of these tumors. The similar pattern of keratinization in these tumors and the similar pattern of beta-catenin immunoreactivity in the cytoplasm and the nucleus are important findings. It seems that the activation of a common cellular pathway, namely Wnt-beta-catenin-TCF-Lef, has a role in the pathogenesis of these tumors. The latter could be related to their shared method of keratinization or shared dysfunction of the cellular adhesion complex leading to tumorigenesis.
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ABSTRACT: Junctional complexes are important in maintaining epithelial cell polarity and cell-cell interactions and are known to be involved in tooth development; thus the purpose of the present study was to investigate the immunohistochemical profile of beta-catenin, gamma-catenin and P-cadherin in 41 epithelial odontogenic lesions (5 radicular cysts, 17 keratocystic odontogenic tumors, 3 dentigerous cysts, 6 calcifying odontogenic cysts, 9 ameloblastomas and one ameloblastic carcinoma). Positive immunostaining was obtained in all cystic lesions as well as in ameloblastomas for the three proteins. Weak staining of beta-catenin and gamma-catenin and absence of P-cadherin expression were observed in ameloblastic carcinoma. These results denote more cytodifferentiation of odontogenic epithelium in ameloblastoma and let us speculate that loss of P-cadherin expression may have a role in transition from benign (ameloblastoma) to malignant phenotype (ameloblastic carcinoma) . Nuclear and cytoplasmic expressions of beta-catenin in half of examined calcifying odontogenic cysts and in ameloblastomas and ameloblastic carcinoma cases suggest deregulation of this protein and reinforce the role of Wnt-beta-catenin- TCF-Lef pathway in the pathogenesis and/or behavior of such lesions.European Journal of Inflammation 04/2011; 9(2 (s)):37-42. · 0.99 Impact Factor
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ABSTRACT: Odontogenic keratocyst is now designated by the World Health Organization as a keratocystic odontogenic tumor (KCOT). According to recent reports Wnt pathway and ß-catenin are involved in the pathogenesis of the majority of odontogenic and neoplastic lesions. The aim of this study was to evaluate the expression of ß-catenin in KCOT and compare it with those of dentigerous cyst and ameloblastoma. Expression of ß-catenin was investigated by immunohistochemistry using specific monoclonal antibodies in 57 formalin-fixed paraffin-embedded samples of KCOT, dentigerous cyst and ameloblastoma (19 samples in each group). The expression of - catenin protein was observed separately in the membrane, cytoplasm and nucleus of epithelial cells. Percentages of expression of membranous, cytoplasmic, and nuclear ß-catenin were 68.4%, 89.5% and 5.3% for KCOT; 78.9%, 100%, and 26.3% for ameloblastoma and 42.1%, 84.2%, and 5.3% for dentigerous cyst, respectively. The expression of membranous ß-catenin in the dentigerous cyst was significantly lower than that in KCOT and ameloblastoma (P<0.05). In other cases, there were no significant statistical differences between the three groups. Membranous expression of ß-catenin might be useful in differentiation of KCOT and ameloblastoma from dentigerous cyst. However, intracellular accumulation of this protein cannot be used to prove the neoplastic nature of KCOT versus dentigerous cyst. Moreover, considering the intracellular accumulation of ß-catenin in most cases in all the three lesions, it seems that ß-catenin changes might play a role in development of odontogenic epithelium in this lesion through deregulation of cell cycle.
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ABSTRACT: HSP27 belongs to the Heat shock protein (HSP) family, which exerts essential functions during the cell cycle under physiological conditions and prevents the stress-induced cellular damage. During the cell development, Hsp27 seem to play a crucial role at different stages, associated with cell proliferation, differentiation and death. Moreover, it seems involved in the balance between differentiation and apoptosis, also during the formation of calcified tissue. The aim of this study was to investigate the expression of HSP27 in odontogenic cysts and its possible biological role. Histological sections of epithelial odontogenic cysts (10 radicular cysts, 8 dentigerous cysts, 16 odontogenic keratocysts) were analyzed for HSP27 expression by immunohistochemistry. All odontogenic cysts were positive for HSP27, although with remarkable differences in the immunostaining pattern according to cyst types. Both proliferating epithelial cell rests and radicular cysts shared an overexpression of HSP27 with concomitant presence of local intraepithelial or subepithelial inflammatory cells. In odontogenic cysts epithelial cells immunolabelling was mainly cytoplasmatic. HSP27 expression may play several roles in the pathogenesis of periapical dental lesions including the induction of epithelial cell rests migration and the increased resistance both to necrosis and apoptosisEuropean Journal of Inflammation 04/2011; 9(2 (s)):33-42. · 0.99 Impact Factor