Molecular analysis of oral carcinogenesis with in vitro multistepcarcinogenesis model

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In this study, we examined the participation and possibility of HPV in oral carcinogenesis. We transduced either HPV16 E6/E7 or a mutant CDK4, cyclinD1, and human telomerase reverse transcriptase (TERT) into primary human tongue keratinocytes. Moreover, additional transduction of oncogenic HRAS or EGFR together with MYC, and dominant negative p53 into immortalized keratinocytes. Furthermore, we examined the incidence of HPV infection and genotype of HPV in oral and cancers in Japanese patients using the biopsy specimens. As results, HPV infection in 21 cases of oral cancer was not detected. Therefore, involvement of HPV infection to oral carcinogenesis was suggested to be less than that in oropharyngeal carcinogenesis in Japan, but HPV infection was caused to oral carcinogenesis.