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Promoter methylation and loss of p16 INK4a gene expression in head and neck cancer
Author(s) -
Demokan Semra,
Chuang Alice,
Suoğlu Yusufhan,
Ulusan Murat,
Yalnız Zubeyde,
Califano Joseph A.,
Dalay Nejat
Publication year - 2012
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.21949
Subject(s) - methylation , gene silencing , carcinogenesis , biology , gene expression , dna methylation , tumor suppressor gene , cancer research , bisulfite sequencing , gene , promoter , cancer , microbiology and biotechnology , genetics
Background Silencing of tumor suppressor genes plays a vital role in head and neck carcinogenesis. In this study we aimed to evaluate aberrant p16 INK4a gene promoter methylation in patients with head and neck cancer. Methods Methylation of the gene was investigated by bisulfite modification/methylation‐specific polymerase chain reaction and gene expression levels were analyzed by quantitative reverse transcription–polymerase chain reaction in tumors and matched normal tissue samples from Turkish patients with head and neck cancer. Results The promoter region of the p16 INK4a gene was methylated in 67.5% and 28.6% of the primary tumors and the corresponding normal tissue, respectively. This difference was highly significant. In concordance, p16 INK4a gene expression was downregulated in 67.5% of the tumor samples. Methylation and the absence of expression in the tumors were observed in 48% of the patients. Conclusions Our data indicate that methylation of the p16 INK4a gene is a frequent event in primary head and neck cancer and that it plays a major role in the silencing of p16 INK4a gene expression during tumor development. © 2011 Wiley Periodicals, Inc. Head Neck, 2011