The role of ATM and H2AX protein expression in oral cavity squamous cell carcinomas

• Main Authors: Kai Lun Cho, 卓楷倫
• Other Authors: S. D. Cheng
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/97015659783958994557

碩士 === 長庚大學 === 生物醫學研究所 === 104 === DNA double-strand break is one of the types of DNA damage, which developed two cell repair mechanisms: homologous recombination and non-homologous end join. Some important tumor suppressor genes are involved in these repairs, such as ATM, Chk2, BRCA1, and BRCA2. In early stage of DNA damage, ATM and other protein kinases phosphorylate H2AX at Ser139 to form γH2AX. ATM and γH2AX overexpress at damage site until the completion of DNA repair. Recent studies indicated that cigarettes, alcohol and betel quid are correlated to oral cancer in Taiwan and smoking leads to DNA damage and DNA mutation which could subsequently play important roles in the process of carcinogenesis. Our purpose is to investigate the role of DNA repair proteins, ATM, pATM and H2AX, in oral cavity squamous cell carcinomas (OSCC). The method to detect protein expression was immunohistochemistry (IHC) staining. Our results showed that ATM was correlated with tumor depth (p = 0.000), tumor stage (p = 0.013) and lymphatic vessel invasion (p = 0.027); pATM was correlated with tumor depth (p = 0.027), tumor size(p = 0.001), tumor stage(p = 0.029), cigarette smoking(p = 0.033), skin invasion (p = 0.014) and bone invasion (p = 0.000); H2AX was correlated with cancer site (p = 0.011), cigarette smoking (p = 0.008) and betel quid chewing (p = 0.012). We also found that ATM was significantly correlated with overall survival (p = 0.023) and also correlated with disease-free survival (p = 0.043) in patients who had adjuvant chemoradiation therapy. ATM, pATM and H2AX play important roles in oral cancer development. The overexpression of ATM could provide survival benefits in OSCC patients in Taiwan.