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Human papillomavirus‐16 DNA methylation patterns support a causal association of the virus with oral squamous cell carcinomas
Author(s) -
BalderasLoaeza Adriana,
AnayaSaavedra Gabriela,
RamirezAmador Velia A.,
GuidoJimenez Miriam C.,
Kalantari Mina,
CallejaMacias Itzel E.,
Bernard HansUlrich,
GarciaCarranca Alejandro
Publication year - 2007
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.22563
Subject(s) - dna methylation , epigenetics , pathology , methylation , etiology , biology , medicine , cancer research , dna , gene , gene expression , genetics
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. © 2007 Wiley‐Liss, Inc.