RESUMO
This report describes the histological and immunohistochemical characteristics of 3 cases of nerve sheath myxoma (NSM)/neurothekeoma arising in the oral cavity. Histopathologically, 3 distinct variants were observed based on the amount of myxoid matrix: classic/hypocellular, cellular, and mixed types. Immunohistochemically, all types expressed strong immunoreactivity to S-100 protein (3/3), NSE (neuron-specific enolase) (3/3), and NGFR (nerve growth factor receptor) (3/3), whereas all cases were negative for SMA (smooth muscle actin) and FVIII. The number of Ki-67 positive cells was less than 5% in all lesions confirming the slow growing characteristics of NSM. The results suggest that NSMs of the oral cavity are true peripheral nerve sheath tumors and show close relationship to schwannoma.
Assuntos
Neoplasias Bucais/patologia , Neurotecoma/patologia , Bochecha/patologia , Pré-Escolar , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Bucais/química , Neurotecoma/química , Fosfopiruvato Hidratase/análise , Receptores de Fator de Crescimento Neural/análise , Proteínas S100/análiseRESUMO
Desmocollin 3 (Dsc3) and desmoglein 3 (Dsg3) are both transmembrane glycoproteins that belong to the cadherin family of calcium-dependent cell adhesion molecules. beta-Catenin is a member of the cadherin-catenin complex that mediates homotypic cell-cell adhesion and is also an important molecule in the wnt signaling pathway. In this study, we examined the simultaneous expression level of Dsc3, Dsg3, and beta-catenin in oral squamous cell carcinomas (OSCCs) and normal oral epithelia using immunohistochemistry. There was a significant correlation (p < 0.05) among the following variables in OSCCs: reduced or loss of expression of Dsc3, Dsg3, and beta-catenin compared to normal oral epithelium, reduced or loss of expression of Dsc3 and histological grade (moderately or poorly differentiated), and reduced or loss of expression of beta-catenin and lymph node metastasis. Furthermore, a positive correlation was found between reduced or loss of beta-catenin staining and reduced or loss of Dsc3 staining in lymph node metastatic cancer tissue (r = 0.734, p < 0.05). These results suggest an abnormal expression of Dsc3, Dsg3, and beta-catenin induced in the progression of oral carcinomas and that the Dsc3 expression level might be related to the regulation of beta-catenin in lymph node metastasis and cell proliferation in OSCCs.
Assuntos
Carcinoma de Células Escamosas/metabolismo , Desmocolinas/biossíntese , Desmogleína 3/biossíntese , Neoplasias Bucais/metabolismo , beta Catenina/biossíntese , Adulto , Idoso , Idoso de 80 Anos ou mais , Carcinoma de Células Escamosas/patologia , Proliferação de Células , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Imuno-Histoquímica , Metástase Linfática/fisiopatologia , Masculino , Pessoa de Meia-IdadeRESUMO
We report an immunohistochemical investigation of the expression of activated extracellular signal-regulated kinase (ERK1/2) and cyclin D1 protein in both oral tongue squamous cell carcinomas (OTSCCs) and normal tongue epithelium. The expression of Ki-67 labeling index (LI) was also examined in order to evaluate cell proliferation activity. The expression of activated ERK1/2, cyclin D1 protein and Ki-67 LI were significantly stronger in OTSCCs than in normal oral mucosa (P<0.05). Both over-expression of activated ERK1/2 and positive expression of Ki-67 in OTSCCs were significantly associated with a moderately or poorly differentiated grade of carcinoma (P<0.05). Cyclin D1 immunostaining showed statistically significant association with both lymph node metastasis (P<0.05) and a tumor thickness >5mm (P<0.05). Over-expression of activated ERK1/2 was positively correlated with cyclin D1 protein expression (P<0.05, r=0.624) and cell proliferation-related indexes Ki-67 (P<0.05, r=0.723). Our results suggest that over-expression of activated ERK1/2 and cyclin D1 protein are involved in oral tongue carcinogenesis, and that activation of ERK1/2 might be related to cell cycle regulation and cell proliferation in OTSCCs.