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Cancer Sci. 2010 Aug;101(8):1891-6. doi: 10.1111/j.1349-7006.2010.01622.x. Epub 2010 May 19.

Prevalence of human papillomavirus 16/18/33 infection and p53 mutation in lung adenocarcinoma.

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1
Division of Biology, National Cancer Center Research Institute, Tokyo, Japan.

Abstract

Human papillomavirus (HPV) infection is a causative event for the development of uterine cervical carcinoma. Human papillomavirus (HPV) 16, 18, and 33 DNA has been also detected frequently in lung adenocarcinomas (AdCs) in East Asian countries; however, its prevalence in Japan remains unclear. We therefore screened for HPV 16/18/33 DNA in 297 lung AdCs in a Japanese population by multiplex PCR with type-specific primers. As reported previously, HPV 16 DNA was detected in two cervical cancer cell lines, CaSki and SiHa, while HPV 18 DNA was detected in HeLa cells, and 0.1-1.0 copies of HPV-DNA per cell were detectable by this method. However, with this method, none of the 297 lung AdCs showed positive signals for HPV 16/18/33 DNA, indicating that HPV-DNA is not or is very rarely integrated in lung AdC genomes in the Japanese. Furthermore, none of the lung AdCs showed positive signals by nested PCR with HPV 16/18 type-specific primers. Therefore, we further attempted to detect HPV 16/18/33 DNA in 91 lung cancer cell lines, including 40 AdC cell lines. Among them, 30 have been established in Japan and the remaining 61 in the USA. No HPV signals were obtained in any of the 91 cell lines by either multiplex or nested PCR, while the p53 gene was mutated in 81 of them including 35 of the 40 AdC cell lines. These results indicate that HPV 16/18/33 infection does not play a major role in the development of lung AdC in Japan nor in the USA.

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