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ORIGINAL ARTICLE
Year : 2018  |  Volume : 14  |  Issue : 6  |  Page : 1180-1183

Immunolocalization of c-Jun in normal mucosa, oral submucous fibrosis, epithelial dysplasia, and oral squamous cell carcinoma: A comparative study


Department of Oral and Maxillofacial Pathology, SDM College of Dental Sciences and Hospital, Dharwad, Karnataka, India

Correspondence Address:
K S Shraddha
SDM College of Dental Sciences and Hospital, Dharwad, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcrt.JCRT_324_16

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Background and Objective: c-Jun an activator protein-1 transcription factor component is activated by a variety of extracellular stimuli. Overexpression of c-Jun has been implicated in the pathogenesis of several types of cancer including oral cancer. The aim of this study was to correlate the expression of c-Jun in the normal buccal mucosa (NM), oral submucous fibrosis (OSMF), severe epithelial dysplasia (ED), and well-differentiated squamous cell carcinoma (WDSCC). Subjects and Methods: Qualitative and quantitative expression of c-Jun was evaluated in a total of 60 histopathologically diagnosed cases, 15 each of NM, OSMF, ED, and WDSCC. The percentage of positive cells (Nuclear labeling index [nLI]) was considered for quantitative assessment and grading of staining for qualitative assessment. Results: The average nLI of c-Jun expression in NM, OSMF, ED, and WDSCC was 35.02%, 35.61%, 89.09%, and 83.31%, respectively. A statistical significant difference was found in c-Jun expression quantitatively between NM and ED (P = 0.000), NM and WDSCC (P = 0.000), OSMF and ED (P = 0.000), OSMF and WDSCC (P = 0.000), and ED and WDSCC (P = 0.021). Qualitatively, statistical significant difference was seen in an intense c-Jun expression between OSMF and ED (P = 0.000), OSMF and WDSCC (P = 0.032), and ED and WDSCC (P = 0.011). Conclusion: The overexpression of c-Jun in ED and WDSCC reveals its role in early carcinogenesis as evidenced in this study. Therefore, c-Jun might act in different mechanisms and pathways which lead to a malignant transformation in oral lesions.


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