| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3166408 | Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology | 2016 | 8 Pages |
ObjectiveOral cancer may be preceded by potentially malignant lesions, and smoking is a risk factor. Oral leukoplakia (OL), which is the most common among these lesions, is defined by the World Health Organization as “a white plaque of questionable risk having excluded known diseases or disorders that carry no increased risk for cancer.” Thus, OL is a clinical diagnosis used to designate oral white lesions, which are histologically represented by hyperkeratosis associated or not associated with epithelial dysplasia. It is known that c-Jun and pc-Jun have a role in cell proliferation and that p27 is decreased during carcinogenesis; thus, the aim of this study was to investigate whether these proteins are differently expressed in OL in smokers and never-smokers.Study DesignSeventy-three cases diagnosed as OL were selected and divided into four groups according to the presence or absence of dysplasia and patients' smoking status (smokers: 39 cases, 24 dysplastic; never-smokers: 34 cases, 20 dysplastic). The immunoexpressions of c-Jun, pc-Jun, and p27 were evaluated.ResultsA significant correlation between smoking condition and the percentages of c-Jun (P = .0356) and pc-Jun (P = .0216) was found and was more intense in cases that underwent malignant transformation (6/47).ConclusionsSmoking habits may be linked to the expression of proteins directly associated with cell cycle progression.
