Human papillomavirus-16 DNA methylation patterns support a causal association of the virus with oral squamous cell carcinomas

被引:40
作者
Balderas-Loaeza, Adriana
Anaya-Saavedra, Gabriela
Ramirez-Amador, Velia A.
Guido-Jimenez, Miriam C.
Kalantari, Mina
Calleja-Macias, Itzel E.
Bernard, Hans-Ulrich [1 ]
Garcia-Carranca, Alejandro
机构
[1] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA
[2] Univ Nacl Autonoma Mexico, Fac Quim, Mexico City 04510, DF, Mexico
[3] Inst Nacl Cancerol SS, Div Invest, Mexico City, DF, Mexico
[4] Univ Autonoma Metropolitana, Mexico City, DF, Mexico
[5] Univ Nacl Autonoma Mexico, Dept Biol Mol & Biotecnol, Inst Invest Biomed, Mexico City 04510, DF, Mexico
关键词
papillomavirus; carcinoma; head and neck cancer; oral cavity; DNA methylation; DNA recombination; etiology; progression; HPV-16;
D O I
10.1002/ijc.22563
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Infection with human papillomavirus-16 (HPV-16) is the cause of most anogenital carcinomas. This virus is also detected in about 20% of all head and neck squamous cell carcinomas. While there is strong evidence for a causal etiological role in the case of tonsillar carcinomas, causal association with malignant lesions of the oral cavity is not yet conclusive. Our previous investigations of HPV-16 DNA methylation in anogenital sites have identified hypermethylation of the L1 gene and part of the long control region in many malignant lesions, but rarely in asymptomatic infections and low-grade precancerous lesions. Here, we report hypermethylation of this diagnostically important segment of the viral DNA in 10 out of 12 HPV-16 positive oral carcinomas from Mexican patients. These data indicate epigenetic changes of HPV-16 in oral carcinomas similar to those in anogenital carcinomas, suggesting carcinogenic processes under the influence of HPV-16 in most if not all of these oral malignant lesions. (c) 2007 Wiley-Liss, Inc.
引用
收藏
页码:2165 / 2169
页数:5
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