B G Bentz1, G K Haines, D G Hanson, J A Radosevich. 1. Department of Otolaryngology-Head and Neck Surgery and the Robert H. Lurie Cancer Center, Northwestern University Medical Center, Chicago, Illinois, USA.
Abstract
BACKGROUND: Nitric oxide (NO.) has been implicated in the process of carcinogenesis in various organs. This study was designed to investigate the expression of endothelial constitutive nitric oxide synthase (ecNOS) in normal and neoplastic salivary tissues. METHODS: Paraffin-embedded tissue from 48 salivary tumors and adjacent non-neoplastic tissue was immunohistochemically evaluated for both frequency (percentage) and intensity (1-4+) of staining using a commercially available anti-ecNOS monoclonal antibody. RESULTS: Expression of ecNOS was predominantly localized to vascular endothelium, skeletal muscle, and to salivary duct luminal epithelium in normal salivary tissue (n = 37). All salivary tumors demonstrated at least 1 + cytoplasmic staining for ecNOS without apparent correlation to most clinical parameters. A tendency toward increased frequency and intensity of ecNOS expression in oncocytic cells, relative to cells with myoepithelial or acinar differentiation, was noted. CONCLUSIONS: Expression of ecNOS is localized to the luminal cells of normal salivary ducts. Limited expression of ecNOS was found in all the salivary gland tumors examined. This suggests a common histogenesis for this diverse group of tumors, which may reflect different degrees of differentiation toward luminal duct epithelium. The possible role of ecNOS and NO. in salivary gland carcinogenesis is intriguing and warrants further study.
BACKGROUND:Nitric oxide (NO.) has been implicated in the process of carcinogenesis in various organs. This study was designed to investigate the expression of endothelial constitutive nitric oxide synthase (ecNOS) in normal and neoplastic salivary tissues. METHODS:Paraffin-embedded tissue from 48 salivary tumors and adjacent non-neoplastic tissue was immunohistochemically evaluated for both frequency (percentage) and intensity (1-4+) of staining using a commercially available anti-ecNOS monoclonal antibody. RESULTS: Expression of ecNOS was predominantly localized to vascular endothelium, skeletal muscle, and to salivary duct luminal epithelium in normal salivary tissue (n = 37). All salivary tumors demonstrated at least 1 + cytoplasmic staining for ecNOS without apparent correlation to most clinical parameters. A tendency toward increased frequency and intensity of ecNOS expression in oncocytic cells, relative to cells with myoepithelial or acinar differentiation, was noted. CONCLUSIONS: Expression of ecNOS is localized to the luminal cells of normal salivary ducts. Limited expression of ecNOS was found in all the salivary gland tumors examined. This suggests a common histogenesis for this diverse group of tumors, which may reflect different degrees of differentiation toward luminal duct epithelium. The possible role of ecNOS and NO. in salivary gland carcinogenesis is intriguing and warrants further study.
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