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논문 기본 정보

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학술저널
저자정보
Khor, Goot Heah (Centre of Preclinical Science Studies, Faculty of Dentistry, Universiti Teknologi MARA, Sungai Buluh Campus) Froemming, Gabrielle Ruth Anisah (Institute of Pathology, Laboratory and Forensic Medicine, Faculty of Medicine, Universiti Teknologi MARA, Sungai Buluh Campus) Zain, Rosnah Binti (Oral Cancer Research and Coordinating Centre, Faculty of Dentistry, University of Malaya) Abraham, Thomas Mannil (Tengku Ampuan Rahimah Hospital, Department of Oral and Maxillofacial Surgery, Ministry of Health Malaysia) Lin, Thong Kwai (Institute of Biological Science, Faculty of Science, University of Malaya)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제17권 제1호
발행연도
2016.1
수록면
219 - 223 (5page)

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Background: Promoter hypermethylation is a frequent epigenetic mechanism for gene transcription repression in cancer and is one of the hallmarks of the disease. Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) contributes to cell contact-mediated communication. Dysregulation of promoter methylation has been reported in various cancers. Objectives: The objectives of this study were to investigate the CELSR3 hypermethylation level in oral squamous cell carcinomas (OSCCs) using methylation-sensitive high-resolution melting analysis (MS-HRM) and to correlate CELSR3 methylation with patient demographic and clinicopathological parameters. Materials and Methods: Frozen tissue samples of healthy subjects' normal mucosa and OSCCs were examined with regard to their methylation levels of the CELSR3 gene using MS-HRM. Results: MS-HRM analysis revealed a high methylation level of CELSR3 in 86% of OSCC cases. Significant correlations were found between CELSR3 quantitative methylation levels with patient ethnicity (P=0.005), age (P=0.024) and pathological stages (P=0.004). A moderate positive correlation between CELSR3 and patient age was also evident (R=0.444, P=0.001). Conclusions: CELSR3 promoter hypermethylation may be an important mechanism involved in oral carcinogenesis. It may thus be used as a biomarker in OSCC prognostication.

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