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p53 and p16 in oral epithelial dysplasia and oral squamous cell carcinoma: A study of 208 cases
Juan C Cuevas Gonzalez1, Luis A Gaitan Cepeda1, Socorro A Borges Yanez2, Alejandro Donohue Cornejo3, Ana D Mori Estevez4, Elba Rosa Leyva Huerta1
1 Graduate and Research Division, Laboratory of Oral Pathology, Dental School, National Autonomous University of, Mexico
2 Department of Oral Public Health, Graduate and Research Division, Dental School, National Autonomous University of , City, Mexico
3 Department of Stomatology, Laboratory of Oral Pathology, Biomedical Sciences Institute, University of Ciudad Juárez, Ciudad Juárez, Mexico
4 Department of Head and Neck Pathology, Hospital Calixto García, Habana, Cuba
Correspondence Address:
Elba Rosa Leyva Huerta
Laboratory of Clinical and Experimental Pathology, Graduate and Research Division, Dental School, National Autonomous University of Mexico, Circuito Institutos s/n, Ciudad Universitaria, Coyoacan, 04510, Mexico City
Mexico
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0377-4929.182037
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Background: The use of p16 and p53 as biomarkers of malignant transformation of oral epithelial dysplasia (OED) and biological behavior of oral squamous cell carcinoma (OSCC) is controversial. Aim: To determine the immunoexpression of p16 and p53 in OED and OSCC and to establish their possible relation to histopathological grading of OED/OSCC. Materials and Methods: Ninety-six OEDs (40 mild, 36 moderate, and 20 severe dysplasia); and 112 OSCCs (64 well-differentiated, 38 moderately differentiated, and 10 poorly differentiated) coming from archives of four centers of oral pathology were included. Histological slides from all cases were processed with immunohistochemical technique using anti-p53 and anti-p16 antibodies. The intensity of the immunoreactivity were classified using the ImageLab®MCM systemas follows: <60 mild, >60–<90 moderate, and >90 strong. Forstatistical purposesa χ2 test (P < 0.05) was performed. Results: Severe dysplasia show highest relative frequency of p16-positive (35.5%), whereas p53 is associated with mild dysplasia (P = 0.04). Moderately differentiated OSCC had larger relative frequency of p16-positive and p53-positive cases (47.3% both circumstances) (P > 0.05). Statistical association of p16-positive and p53-positive cells to basal stratum of OED (P = 0.0008; P = 0.0000, respectively) and p16-positive cells and p53-positive cells to perivascular zone of OSCC (P = 0.001; P = 0.0000, respectively) was found. Conclusions: p16 and p53 could be not specific enough to identify patients suffering OED with high risk to malignancy; however, the evaluation of the presence of p16 and p53 in the tumoral invasive front of OSCC could contribute to establish the tumor progression. |
