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

Prevalence of human papillomavirus 16/18/33 infection and p53 mutation in lung adenocarcinoma
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DOI:
10.1111/j.1349-7006.2010.01622.x
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发表时间:
2010-08-01
期刊:
影响因子:
5.7
通讯作者:
Yokota, Jun
Yokota, Jun
中科院分区:
医学2区
文献类型:
--
作者:
Iwakawa, Reika;Kohno, Takashi;Yokota, Jun

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人乳头瘤病毒(HPV)感染是宫颈癌发展的一个致病事件。在东亚国家的肺腺癌(adc)中也经常检测到人乳头瘤病毒(HPV) 16、18和33的DNA;然而,它在日本的流行程度尚不清楚。因此,我们在日本人群的297例肺adc中通过多重PCR与类型特异性引物筛选HPV 16/18/33 DNA。此前报道,在CaSki和SiHa两种宫颈癌细胞系中检测到HPV 16 DNA,而在HeLa细胞中检测到HPV 18 DNA,每个细胞检测到0.1-1.0拷贝的HPV-DNA。然而,通过这种方法,297例肺AdC中没有一例显示HPV 16/18/33 DNA阳性信号,这表明HPV-DNA没有或很少整合到日本肺AdC基因组中。此外,用HPV 16/18型特异性引物巢式PCR检测,所有肺adc均未显示阳性信号。因此,我们进一步尝试在91个肺癌细胞系中检测HPV 16/18/33 DNA,其中包括40个AdC细胞系。其中30家在日本成立,其余61家在美国。通过多重或巢式PCR, 91个细胞系均未获得HPV信号,而p53基因在81个细胞系中发生突变,其中包括40个AdC细胞系中的35个。这些结果表明,HPV 16/18/33感染在日本和美国的肺AdC的发展中并不起主要作用。(癌症科学2010;101:1891-1896)
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. (Cancer Sci 2010; 101:1891-1896)