Molecular analysis of oral carcinogenesis with in vitro multistepcarcinogenesis model

在这项研究中，我们研究了HPV在口腔癌变中的参与和可能性。我们将HPV16 E6/E7或突变体CDK4、cyclinD1和人端粒酶逆转录酶（TERT）转导到原代人舌角化细胞中。此外，致癌HRAS或EGFR与MYC和显性阴性p53一起转导成永活的角化细胞。此外，我们使用活检标本检测了日本口腔和癌症患者中HPV感染的发生率和HPV基因型。结果21例口腔癌未检出HPV感染。因此，HPV感染对口腔癌变的参与程度低于日本的口咽癌变，但HPV感染导致了口腔癌变。

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.