Activation Induced cytidine Deaminase (AID) has been shown as an endogenous mutator when its expression was not controlled. AID acts directly on the tumor suppressor genes by accumulating mutations gradually resulted in inactivation and loss of their function. p53 is a frequent target for genetic alteration in various human malignancies. The aim of this study was to examine the involvement of AID in the development of human HCC. The results indicated that: (1). AID actin transcriptional ratio in the liver cancer tissues and in the liver cirrhosis tissue were 11.09 + or - 4.73 and 7.87 + or - 1.97, while and AID actin ratio in the chronic hepatitis tissue was 2.18 + or - 0.75, respectively. (2). Subsequently, mutation frequency in p53 gene from liver cancer tissue, liver cirrhosis tissue were 17.8 percent, and 2.2 percent and no detected in the chronic hepatitis tissues. (3). AID trancriptional ratio with p53 gene mutation in the liver tissue is 9.36 + or - 3.13, AID trancriptional ratio with no p53 gene mutation in the liver tissue is 9.39 + or - 5.3 ( P 0.05). Taken together, our results indicated that AID upregulation in the enhancement of genetic susceptibility to mutagenesis, leading to the development of HCC in the setting of chronic liver. Howerver, no significant difference was found in AID transcripts in mutated and non-mutated p53 gene.
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