Promoter methylation and loss of p16INK4a gene expression in head and neck cancer

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Demokan S., Chuang A., Suoglu Y., Ulusan M., Yalnız Z., Califano J. A., ...Daha Fazla

HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK, cilt.34, sa.10, ss.1470-1475, 2012 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 34 Sayı: 10
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1002/hed.21949
  • Dergi Adı: HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.1470-1475
  • Anahtar Kelimeler: p16INK4a, head and neck cancer, methylation, expression, SQUAMOUS-CELL CARCINOMA, TUMOR-SUPPRESSOR GENE, HUMAN HEPATOCELLULAR-CARCINOMA, PROTEIN EXPRESSION, P16 GENE, COLORECTAL-CANCER, DNA METHYLATION, BREAST-CANCER, MICROSATELLITE INSTABILITY, CLINICAL-IMPLICATIONS
  • İstanbul Üniversitesi Adresli: Evet

Özet

Background Silencing of tumor suppressor genes plays a vital role in head and neck carcinogenesis. In this study we aimed to evaluate aberrant p16INK4a 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 p16INK4a 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, p16INK4a 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 p16INK4a gene is a frequent event in primary head and neck cancer and that it plays a major role in the silencing of p16INK4a gene expression during tumor development. (c) 2011 Wiley Periodicals, Inc. Head Neck, 2011