【摘 要】
：
目的:流行病学调查表明,慢性乙型肝炎病毒(Hepatitis B virus,HBV)的感染是原发性肝细胞癌(hepatocellular cell carcinoma,HCC)发生的独立危险因素.在慢性持续性的HBV感染中,HBV DNA可整合入人体基因组.有文献报道,HBV整合入宿主肝细胞最基本的效应是诱发基因组的不稳定性,导致宿主染色体序列缺失、重排,基因结构和表达异常不断积累,最终导致细胞
【机 构】
：
第二军医大学基础部医学遗传学教研室,上海,200433 第二军医大学东方肝胆医院,上海,20043
【出 处】
：
2014全球华人遗传学大会暨全国第十三次医学遗传学学术会议
论文部分内容阅读
目的:流行病学调查表明,慢性乙型肝炎病毒(Hepatitis B virus,HBV)的感染是原发性肝细胞癌(hepatocellular cell carcinoma,HCC)发生的独立危险因素.在慢性持续性的HBV感染中,HBV DNA可整合入人体基因组.有文献报道,HBV整合入宿主肝细胞最基本的效应是诱发基因组的不稳定性,导致宿主染色体序列缺失、重排,基因结构和表达异常不断积累,最终导致细胞恶性转化及克隆性生长.HBV相关的HCC标本中,高达85％的HCC细胞基因组中可检测到病毒DNA的整合,且HCC组织中HBV基因组的整合次数要比癌旁组织显著增加.在过去的研究中,关于病毒整合的机制和意义的研究已取得一定进展,但仍存在一些重要的问题没有解决,如优势整合位点的选择性及"基因荒漠区域"整合位点的功能意义等.
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