DNA content, Cyclooxygenase-2 expression and loss of E-cadherin expression do not predict risk of malignant transformation in oral lichen planus
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Oral lichen planus (OLP) may be associated with a small risk of malignant transformation of the oral mucosa. Using cases which had transformed, and those which had not, this study aimed to evaluate the potential of DNA content, expression of Cyclooxygenase-2 (Cox-2) and of epithelial (E)-cadherin as risk markers in lesions of OLP. We investigated 78 archival biopsies from; (1) 26 OLP patients with at least two biopsies, of whom seven presented OLP with epithelial dysplasia, followed by oral squamous cell carcinoma (OSCC) in five of them, (2) 19 OLP patients with one biopsy taken. Image cytometry for measurement of DNA content and immunohistochemistry for visualisation of Cox-2 and E-cadherin expression were performed. All OLP biopsies investigated were classified as diploid, one OLP with epithelial dysplasia was tetraploid and all OSCC were diploid. Cox-2 was detected in the epithelium of all OLP specimens investigated, as well as in epithelial dysplasias and OSCC. Focal loss of E-cadherin expression was observed in basal keratinocytes in 88% of the OLP specimens investigated, in all epithelial dysplasias and OSCC. In conclusion, neither aneuploidy, Cox-2 expression, nor loss of E-cadherin expression, were significant reliable markers to select OLP lesions at risk for development of OSCC in the present patient material.
KeywordsOral lichen planus Nuclear DNA content Aneuploid Diploid Cox-2 E-cadherin
List of abbreviations
Bovine serum albumin
Oral lichen planus
Oral squamous cell carcinoma
Special thanks to Ruth Puntervold for skilful help in preparation of samples as well as DNA image cytometry analysis and to Bjørn Risberg and Håvard E. Danielsen for classification of the histograms in the DNA cytometry series. Thanks to Marta Kot, Gunnvor Øijordsbakken and Gudveig Fjell for skilful help in the laboratory. We also wish to thank Knut Tornes for help in selecting OLP biopsies from patients that developed epithelial dysplasias and OSCC over years. This work has been supported by grants from University of Bergen and Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway.
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