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  Vol. 131 No. 8, August 2005 TABLE OF CONTENTS
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{beta}-Catenin and Cyclin D1 in Mucoepidermoid Carcinoma of Variable Histologic Grades

Márcia Cristina da Costa Miguel, MSc; Márcio Campos Oliveira, MSc; Flávio Roberto Guerra Seabra, MSc; Lélia Maria Guedes Queiroz, PhD; Roseana de Almeida Freitas, PhD; Lélia Batista de Souza, PhD

Arch Otolaryngol Head Neck Surg. 2005;131:701-706.

Objective  To analyze the expression of {beta}-catenin and cyclin D1 in mucoepidermoid carcinoma (MEC) of variable histologic grades to establish a correlation between the expression of these proteins and the different histopathologic grades of this neoplasia.

Design  Immunohistochemical analysis of MEC.

Setting  Pathological Anatomy Service, Discipline of Oral Pathology, Department of Dentistry, Federal University of Rio Grande do Norte, Natal, Brazil.

Patients  Fifteen cases of MEC, graded and categorized according to criteria reported in the literature into 5 tumors with a low grade of malignancy, 4 with an intermediate grade, and 6 with a high grade.

Main Outcome Measures  Labeling patterns of {beta}-catenin and cyclin D1.

Results  No significant difference in {beta}-catenin labeling patterns was observed between low- and intermediate-grade tumors or between low- and high-grade tumors (P = .60 and P = .06, respectively; Fisher exact test), despite a strong tendency toward a difference in the latter. In contrast, a significant difference was noted between intermediate- and high-grade tumors (P = .03). For cyclin D1, no labeling was observed in any high-grade cases, and only 3 cases showed overexpression of this protein. Comparison of the labeling patterns among the different histologic grades revealed no significant difference.

Conclusions  The reduced expression of {beta}-catenin observed in all high-grade MECs is probably due to the loss of its adhesion function, which confers a greater invasive potential to these tumors. The overexpression of cyclin D1 observed in only 3 MEC cases suggests that this protein does not participate in the etiopathogenesis of these tumors, which implies that other genes are likely responsible.


Author Affiliations: Laboratory of Oral Pathology, Dentistry School, Federal University of Rio Grande do Norte, Natal (Ms Miguel, Messrs Oliveira and Seabra, and Drs Queiroz, Freitas, and de Souza); and State University of Feira de Santana, Bahia (Mr Oliveira), Brazil.



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