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Journal of Histochemistry and Cytochemistry, Vol. 51, 1291-1297, October 2003, Copyright © 2003, The Histochemical Society, Inc.

ARTICLE

p16INK4A Immunohistochemical Overexpression in Premalignant and Malignant Oral Lesions Infected with Human Papillomavirus

Paula Andrea Gabrielli Fregonesia, Debora Barreto Teresaa, Roberta Aparecida Duartea, Carlos Benatti Netob, Maria Rita Brancini de Oliveirab, and Christiane Pienna Soaresa
a Department of Clinical Analysis, Faculty of Pharmaceutical Sciences, University of São Paulo State, Brazil
b Department of Physiology and Pathology, School of Dentistry, University of São Paulo State, Brazil

Correspondence to: Christiane Pienna Soares, Dept. of Clinical Analysis, Faculty of Pharmaceutical Sciences, University of São Paulo State (UNESP), Rua Expedicionários do Brasil 1612, Centro, 14 801 902 Araraquara, São Paulo, Brazil. E-mail: soarescp@hotmail.com

Human papillomavirus (HPV) is believed to promote the oncogenic process, and the correlation between viral oncoproteins and dysfunction of p16INK4A tumor suppressor protein in oral lesions is controversial. To test the hypothesis that anogenital HPV types participate in disruption of the regulation of p16INK4A suppressor protein in oral lesions, we analyzed 46 oral biopsy specimens for the presence of HPV 6/11 and 16/18 by in situ hybridization (ISH) and for p16INK4A expression by immunohistochemistry (IHC). Eighteen (39%) of the 46 oral lesions were HPV-positive and 28 (61%) were HPV-negative. HPV 6/11 DNA was found in 5 (11%) and HPV 16/18 in 13 (28%) of 46 biopsies. Nine of the 18 HPV-positive oral lesions (50%), assessed by catalyzed signal amplification coupled to ISH (CSA–ISH), gave high-intensity p16INK4A immunostaining. Focal and diffuse patterns were observed in 11/13 (77%) lesions with HPV 16/18, focal immunopositivity in 3/5 (80%) with HPV 6/11, and negative or sporadic p16-labeling in 18/28 (64%) without the presence of HPV DNA. These results showed a strong association between overexpression of p16 protein and malignant oral lesions, mainly those infected by HPV 16/18. We can conclude that high-risk HPV types are associated with p16 overexpression, and p16 may serve as a biomarker in oral cancer related to high-risk HPV infection. (J Histochem Cytochem 51:1291–1297, 2003)

Key Words: HPV, oral cancer, p16INK4A, immunohistochemistry, in situ hybridization


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