lation is related to many steps of oral cancer carcinogenesis. This study was conducted to evaluate the expression of the p53 and Rb proteins in malignant and ...
MOLECULAR MEDICINE REPORTS 6: 163-166, 2012
Retinoblastoma and p53 protein expression in pre-malignant oral lesions and oral squamous cell carcinoma MARÍLIA GERHARDT DE OLIVEIRA1, LUCIANA MARIA PEREIRA RAMALHO2, LEONILSON GAIÃO3, DANIEL HUMBERTO POZZA4 and RAMON ANDRADE DE MELLO5,6 1
Department of Maxillofacial Surgery, School of Dentistry, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre; 2 Department of Pathology, School of Dentistry, Federal University of Bahia, Salvador; 3 Department of Maxillofacial Surgery, School of Dentistry, Federal University of Maranhao, Imperatriz, Brazil; 4 Department of Experimental Biology, São João Hospital, Faculty of Medicine, University of Porto; 5 Department of Medical Oncology, Portuguese Oncology Institute; 6Department of Medicine, São João Hospital, Faculty of Medicine, University of Porto, Porto, Portugal Received January 19, 2012; Accepted April 10, 2012 DOI: 10.3892/mmr.2012.876
Abstract. The retinoblastoma (Rb) and p53 genes play a fundamental role in cell cycle mechanisms, and their deregulation is related to many steps of oral cancer carcinogenesis. This study was conducted to evaluate the expression of the p53 and Rb proteins in malignant and pre-malignant oral cavity lesions. This retrospective study was conducted at the Federal University of Bahia, Salvador, Brazil, and the Molecular Biology Laboratory of the Otorhinolaryngology Department at the University of Heidelberg, Heidelberg, Germany. Excisional biopsy samples of oral cavities were collected from patients with suspected oral lesions. The samples were processed by immunohistochemistry to be classified by a semi-quantitative score: samples with a ≤10% positivity were considered to have weak/negative expression (-); those with 11-50% positivity, moderate expression (+); and those with >50% positivity, high expression (++). Seventy-one patients were studied (75% male; median age, 52 years; range, 24-84). Of the samples studied, 59.4% were oral squamous cell carcinoma (OSCC) and 40.6% were pre-neoplastic lesions (leukoplakia and actinic cheilitis). OSCC presented higher expression of Rb protein compared to pre-malignant lesions: 75 vs. 25% (p50%, strong expression (++). Statistical analysis. Data were analyzed according to descriptive statistics, means were compared using parametric and non-parametric tests according to the studied variable and proportions were compared by the Chi-square or Fisher's tests using the Statistical Package for Social Sciences (SPSS), version 19.0, software. A p-value 75% of mature cells) Invasive pattern
Inflamatory infiltrate
Moderately keratinized (20-50% of cells) Moderate nuclear pleomorphism (50-75% mature cells)
Minimum keratinization No keratinization (5-20% of cells) (0-5% of cells) Nuclear pleomorphism abundant (25-50% mature cells)
Extreme nuclear pleomorphism (0-25% mature cells)
Low
Absent
Invasion by tumor edge Invasion through beams, Invasion by cords or Diffuse invasion of single cells large and well-delineated solid bands or cords small groups (>15 cells) or small groups (0.8), were not possible to control. Also, the group of patients was not followed-up due to logistic reasons and, therefore, we could not ensure considerations concerning prognosis and therapeutic response. In conclusion, the paramount expression of these cellular cycle biomarkers (p53 and Rb protein) in excisional biopsies may suggest that molecular lesion assessment plays a role in pre-malignant lesions. Also, p53 protein expression may be related to the early steps of carcinogenesis in OSCC, and a higher Rb protein expression was observed in malignant lesions. Therefore, larger prospective studies are warranted in order to further assess the feasability of using the p53 and Rb proteins as putative prognostic or predictive biomarkers for OSCC. Acknowledgements This study was supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPQ-Brazil), and the University of Heidelberg, Germany. References 1. Jemal A, Bray F, Center M, Ferlay J, Ward E and Forman D: Global cancer statistics. CA Cancer J Clin 61: 69-90, 2011. 2. Jemal A, Siegel R, Xu J and Ward E: Cancer statistics, 2010. CA Cancer J Clin 60: 277-300, 2010.
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