4.2 Article

CD133 expression in oral lichen planus correlated with the risk for progression to oral squamous cell carcinoma

Journal

ANNALS OF DIAGNOSTIC PATHOLOGY
Volume 17, Issue 6, Pages 486-489

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.anndiagpath.2013.06.004

Keywords

CD133; Cancer stem cell marker; Oral lichen planus; Malignant progression; Oral cancer

Categories

Funding

  1. Shanghai Natural Science Foundation [13ZR1436100]

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Oral lichen planus (OLP) is a potentially malignant disorder associated with an increased risk for progression to oral squamous cell carcinoma (OSCC). The objective of this study to determine protein expression of cancer stem cell marker CD133 in tissue samples of patients with OLP and evaluate the correlation between CD133 expression and the risk of progression to OSCC. In this longitudinal case-control study, a total of 110 patients with OLP who received a mean follow-up of 56 months were enrolled, including 100 patients who did not progress to OSCC and 10 patients who had progressed to OSCC. CD133 expression was determined using immunohistochemistry in samples from these patients. Analysis of 10 cases of normal oral mucosa and 6 cases of postmalignant OSCC form previously diagnosed OLP was also performed. The results showed that CD133 expression was observed in 29% cases of nonprogressing OLP and in 80% cases of progressing OLP (P = .002). CD133 was not expressed in normal oral mucosa, but it positively expressed in the 100% cases of OSCC. Logistic regression analysis revealed that the risk of malignant progression in the patients with CD133-positive expression was significantly higher than those with CD133 negativity (odds ratio, 9.79; 95% confidence interval, 1.96-48.92; P = .005). Collectively, CD133 expression was significantly associated with malignant progression in a longitudinal series of patients with OLP. Our findings suggested that CD133 may serve as a novel candidate biomarker for risk assessment of malignant potential of OLP. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.

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