Abstract
Genetic analyses of human mucoepidermoid carcinoma (MEC) revealed that the t(11; 19) (q21; p13) is responsible for its tumorigenesis during which the gene resulting from the fusion between Mammalian Mastermind like 2 and Mucoepidermoid carcinoma translocated 1 activates Hairy/Enhancer of split homologue 1 (HES1), a downstream of the Notch signal. However, in the previous studies, limited clinical cases (15 in total) were investigated for the translocation and HES1 expression. We examined the relevance of aberrant expression of HES1 in 40 cases of MEC and found that 30% of the cases showed the positive signal. No direct relationship of HES1 to the tumor malignancy grade measured by the AFIP score or to the cell proliferation rate was observed although HES1 positive cells were mostly squamous cells. We investigated 12 pleomorphic adenomas and 3 adenoid cystic carcinomas, but they were negative for HES1immunoreactivity with only one exceptional case in pleomorphic adenoma. On the contrary, 5 out of 6 cases of Warthin's tumor showed positive immunoreactivity in the epithelial component. Thus, HES1 expression may regulate specific differentiation of the salivary gland tumor cells, but not tumorigenesis.
