Collagen XVIII modulation is altered during progression of oral dysplasia and carcinoma.

BACKGROUND Collagen XVIII is a ubiquitous basement membrane (BM) component and a precursor of endostatin. METHODS Using immunohistochemistry and in situ hybridization, we studied the expression and localization of collagen XVIII in different stages of normal oral wound healing, epithelial dysplasia and squamous cell carcinoma (SCC). RESULTS In mild epithelial dysplasias collagen XVIII appeared as a continuous signal in the BM, whereas in severe epithelial dysplasias and in the invasive areas of oral SCCs collagen XVIII was absent. In situ hybridization showed that collagen XVIII mRNA expression did not decrease in severe dysplasia or oral carcinoma samples when compared with the mild dysplasias. CONCLUSIONS The results indicate that the absence of collagen XVIII protein in severe oral dysplasias is related to the processing of the protein rather than to changes in mRNA expression.

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