Kai-Ping Chang1,2,3, Chun-I Wang1, Curtis R Pickering4, Yenlin Huang5, Chi-Neu Tsai6, Ngan-Ming Tsang7, Huang-Kai Kao8,3, Ming-Huei Cheng8,3, Jeffrey N Myers4. 1. Department of Otolaryngology - Head and Neck Surgery, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan. 2. Molecular Medicine Research Center, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. 3. College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. 4. Department of Head and Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas. 5. Department of Pathology, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan. 6. Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan. 7. Department of Radiation Oncology, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan. 8. Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan.
Abstract
BACKGROUND: Mutations in the human telomerase reverse transcriptase (TERT) promoter contribute to increased TERT activity. The purpose of the present study was to assess the prevalence of TERT promoter mutations in oral cavity squamous cell carcinoma (SCC). METHODS: Total DNA was extracted from 201 oral cavity SCC tumors and adjacent normal tissues. Primers were used to amplify the sequence region containing 2 TERT promoter mutations (C228T and C250T) that were then sequenced using the Sanger method. RESULTS: Sequencing revealed that 52.5% (104/201) and 12.9% (26/201) of oral cavity SCC tumor tissues and 6.0% (12/201) and 2.5% (5/201) of adjacent normal tissues contained C228T and C250T mutations, respectively. In addition, the C228T mutation was significantly associated with betel nut chewing. CONCLUSION: Our results show that mutations in the TERT promoter occur in patients with oral cavity SCC at a high frequency. This suggests that somatic TERT promoter mutations could play a vital role in the pathogenesis and progression of oral cavity SCC.
BACKGROUND: Mutations in the humantelomerase reverse transcriptase (TERT) promoter contribute to increased TERT activity. The purpose of the present study was to assess the prevalence of TERT promoter mutations in oral cavity squamous cell carcinoma (SCC). METHODS: Total DNA was extracted from 201 oral cavity SCC tumors and adjacent normal tissues. Primers were used to amplify the sequence region containing 2 TERT promoter mutations (C228T and C250T) that were then sequenced using the Sanger method. RESULTS: Sequencing revealed that 52.5% (104/201) and 12.9% (26/201) of oral cavity SCC tumor tissues and 6.0% (12/201) and 2.5% (5/201) of adjacent normal tissues contained C228T and C250T mutations, respectively. In addition, the C228T mutation was significantly associated with betel nut chewing. CONCLUSION: Our results show that mutations in the TERT promoter occur in patients with oral cavity SCC at a high frequency. This suggests that somatic TERT promoter mutations could play a vital role in the pathogenesis and progression of oral cavity SCC.
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