and alcohol-consumption (p = 0.001 and p = 0.007, respectively) anda higher T-stage (p = 0.03). Both HPV-positivity and chromosomedisomy were significantly associated with favorable prognosis(p = 0.003 and p = 0.011, respectively). Five out of six HPV-positive,tumor-adjacent dysplasias also showed disomy for chromosomes 1and 7.

In conclusion, HPV-positive TSCCs and their precursor lesions aregenetically more stable than HPV-negative lesions, suggesting thatHPV integration preferentially occurs in (near) diploid lesions. Thehigh chromosome 7 copy numbers in HPV-negative tumors maypoint to oncogene involvement such as EGFR, which is inverselyrelated to HPV presence. Furthermore, HPV-positivity and chromo-some disomy are favorable prognosticators in TSCC.

doi:10.1016/j.oos.2009.06.276

O192. Double demonstration of oncogenic HPV DNA and HPV-E7protein in 8.57% of oral cancers. Preliminary reportG. Pannone a,b,c,*, P. Bufo a, A. Santoro a, S.M. Papagerakis e, C. Rubini d,L. Lo Muzio a

a University of Foggia, Italyb University of Naples, Italyc University of Palermo, Italyd University of Ancona, Italye University of Michigan, United States

Background: Oncogenic HPVs are necessarily involved in cervicalcancer but their role in oral carcinogenesis is debated. The frequencyof their isolation from oral cancer is largely variable according to dif-ferent studies. The involvement of a virus in carcinogenesis is dem-onstrated after its integration in host DNA with consequentexpression of oncogenic proteins.

Aim: To detect HPV in oral cancer, perform genotyping and dem-onstrate the oncogenic proteins in oral cancer cells.

Materials and methods: Forty-four cases of formalin fixed-paraf-fin embedded OSCC were studied by both DNA genotyping (MY09/11L1 consensus primers in combination with GP5-GP6 primer pair fol-lowed by sequencing) and immunohistochemistry (monoclonal Absagainst capsid protein and HPV-E7 protein, K1H8 DAKO and clone8C9 INVITROGEN, respectively). HPV-16 tonsil cancer was used aspositive control.

Results: The overall prevalence of HPV infection was 14.28%.Amplification of DNA samples showed single HPV DNA infection intwo cases (HPV 53; HPV-70) and double infection in one case(HPV-31/HPV-44) with an oncogenic HPV prevalence of 8.57%. E-7antigen was immunohistochemically detected in all HPV-positivecases.

Discussion: HPVs exert their oncogenic role after DNA integra-tion, gene expression of E5, E6 and E7 loci and p53/pRb host proteinssuppression. This study showed that HPV-E7 protein inactivatingpRb is expressed in oral cancer cells infected by oncogenic HPV otherthan classical HPV-16/18. Interestingly HPV-70, considered a lowrisk virus with no definite collocation in oncogenic type category,gives rise to the expression of HPV-E7 protein and inactivate pRbin oral cancer. HPV-70, as proved in current literature, is able to inac-tivate also p53 protein, promoting cell immortalization. HPV-53,classified as a possible high risk virus, expresses E7 protein in OSCC,contributing to oral carcinogenesis.

We have identified among OSCCs, a subgroup characterized byHPV infection (8.57%): a percentage value not so conspicuous asshown by other Authors. Finally, we have proved the oncogenicpotential of some HPV virus types, which is not well known in theliterature.

doi:10.1016/j.oos.2009.06.277

O193. HPV Identification and immunohistochemical expressionof retinoblastoma pathway proteins in oral carcinogenesisR. Acay *, S.O.M. de Sousa

University of São Paulo, Brazil

Introduction: It is accepted that human papillomavirus (HPV) iscapable of inducing carcinogenesis in uterine cervix, by the interac-tion of its oncoproteins with cell cycle regulatory proteins, mainlythrough p53 and the retinoblastoma pathway. However, it is notyet clear whether HPV is capable of inducing the same phenomenonin the oral cavity. Hence, the aim of this study was to identify theprevalence of HPV in malignant and potentially malignant oral le-sions and to verify its interaction with proteins of the retinoblastomapathway.

Material and methods: Fifty cases diagnosed as oral leukoplakia,with several degrees of epithelial dysplasia, and as oral squamouscell carcinoma and fifty control-cases, represented by oral mucosa– normal or presenting minor histological alterations – were se-lected. Cases were submitted to HPV detection and genotyping byin situ hybridization with signal amplification and also to immuno-histochemical reaction to cyclin D1 and pRb proteins, using the ste-ptoavidin-biotin method.

Results: HPV overall prevalence in the oral lesions was 24%,markedly higher than in the control group (4%) and, in most of thepositive cases (58.3%), presence of high-risk HPV genotypes was de-tected. However, no correlation was observed between the virusdetection and cyclin D1 (p = 0.1902) and pRb (p = 0.9994)expression.

Discussion: Results suggest that HPV does not induce oral car-cinogenesis by the interaction with proteins of the retinoblastomapathway. However, the higher prevalence of high-risk HPV typesin malignant and potentially malignant oral lesions compared withoral normal mucosa does not allow us to discharge HPV as a riskfactor in this context, suggesting that the virus could induce oralcarcinogenesis by interacting with other cell cycle regulatingproteins.

doi:10.1016/j.oos.2009.06.278

O194. HPV Detection in head and neck cancer using the rochelinear array HPV genotyping testJ. Machado a,b,*, P.P. Reis b, T. Zhang b, C. Simpson b, W. Xu b,B. Perez-Ordonez b

a University of Toronto, Canadab University Health Network, Canada

Head and neck squamous cell carcinomas (HNSCCs) are malig-nancies of the oral and nasal cavity, lip, pharynx, and larynx. Riskfactors include tobacco and alcohol abuse and increasing evidenceshows that Human Papillomavirus (HPV) infection can also be asso-ciated with particular HNSCC subtypes. We assessed HPV involve-ment in HNSCC using the Roche Linear Array HPV Genotyping Test,which can detect 37 different HPV types. In a pilot study, we firstcompared this test with PCR detection of HPV in formalin fixed par-affin embedded (FFPE) tissue and observed a concordance of 95%between the two methods. The Roche linear array was able to iden-tify HPV genotypes that were not commonly observed in HNSCC. Wethen examined the prevalence of HPV infection in 71 fresh frozen

120 Oral abstracts / Oral Oncology Supplement 3 (2009) 56–122

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