title: p53 and p16 in oral epithelial dysplasia and oral squamous cell carcinoma: A study of 208 cases.
abstract: 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.
  
  
  OBJECTIVE
  To determine the immunoexpression of p16 and p53 in OED and OSCC and to establish their possible relation to histopathological grading of OED/OSCC.
  
  
  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.
authors.affiliation: Graduate and Research Division, Laboratory of Oral Pathology, Dental School, National Autonomous University of, Mexico.
authors.forename: Juan C
authors.initials: JC
authors.lastname: Cuevas Gonzalez
authors.affiliation: Graduate and Research Division, Laboratory of Oral Pathology, Dental School, National Autonomous University of, Mexico.
authors.forename: Luis A
authors.initials: LA
authors.lastname: Gaitan Cepeda
authors.affiliation: Department of Oral Public Health, Graduate and Research Division, Dental School, National Autonomous University of , City, Mexico.
authors.forename: Socorro A
authors.initials: SA
authors.lastname: Borges Yanez
authors.affiliation: Department of Stomatology, Laboratory of Oral Pathology, Biomedical Sciences Institute, University of Ciudad Juárez, Ciudad Juárez, Mexico.
authors.forename: Alejandro Donohue
authors.initials: AD
authors.lastname: Cornejo
authors.affiliation: Department of Head and Neck Pathology, Hospital Calixto García, Habana, Cuba.
authors.forename: Ana D
authors.initials: AD
authors.lastname: Mori Estevez
authors.affiliation: Graduate and Research Division, Laboratory of Oral Pathology, Dental School, National Autonomous University of, Mexico.
authors.forename: Elba Rosa Leyva
authors.initials: ER
authors.lastname: Huerta
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000032:analysis; D001706:Biopsy; D002294:Carcinoma, Squamous Cell / Q000175:diagnosis / Q000473:pathology*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000175:diagnosis / Q000473:pathology*; D012680:Sensitivity and Specificity; D016159:Tumor Suppressor Protein p53 / Q000032:analysis*
chemical_list: D014408:Biomarkers, Tumor; C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016159:Tumor Suppressor Protein p53