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Effects of AFP-activated PI3K/Akt signaling pathway on cell proliferation of liver cancer.甲胎蛋白激活的PI3K/Akt信号通路对肝癌细胞增殖的影响。
Tumour Biol. 2014 May;35(5):4095-9. doi: 10.1007/s13277-013-1535-z. Epub 2014 Jan 15.
2
Accumulation of the mutations in basal core promoter of hepatitis B virus subgenotype C1 increase the risk of hepatocellular carcinoma in Southern China.乙型肝炎病毒C1亚基因型基础核心启动子区突变的积累增加了中国南方肝细胞癌的发病风险。
Int J Clin Exp Pathol. 2013 May 15;6(6):1076-85. Print 2013.
3
Epidemiology of viral hepatitis and hepatocellular carcinoma.病毒性肝炎与肝细胞癌的流行病学。
Gastroenterology. 2012 May;142(6):1264-1273.e1. doi: 10.1053/j.gastro.2011.12.061.
4
AFP in OLT for HCC?: Another shadow on the cave wall: Comment on "Evaluation of absolute serum α-fetoprotein levels in liver transplant for hepatocellular cancer".肝癌肝移植中的甲胎蛋白?:洞壁上的另一道阴影:评《肝细胞癌肝移植中血清甲胎蛋白绝对值的评估》
Arch Surg. 2011 Jan;146(1):33-4. doi: 10.1001/archsurg.2010.280.
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Global cancer statistics.全球癌症统计数据。
CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90. doi: 10.3322/caac.20107. Epub 2011 Feb 4.
6
Hepatitis B virus x protein in the pathogenesis of hepatitis B virus-induced hepatocellular carcinoma.乙型肝炎病毒 X 蛋白在乙型肝炎病毒诱导的肝细胞癌发病机制中的作用。
J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:144-52. doi: 10.1111/j.1440-1746.2010.06546.x.
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Molecular biology of the hepatitis B virus and role of the X gene.乙型肝炎病毒的分子生物学及X基因的作用
Pathol Biol (Paris). 2010 Aug;58(4):267-72. doi: 10.1016/j.patbio.2010.03.005. Epub 2010 May 18.
8
A mutant of hepatitis B virus X protein (HBxDelta127) promotes cell growth through a positive feedback loop involving 5-lipoxygenase and fatty acid synthase.乙型肝炎病毒 X 蛋白(HBxDelta127)突变体通过涉及 5-脂氧合酶和脂肪酸合酶的正反馈环促进细胞生长。
Neoplasia. 2010 Feb;12(2):103-15. doi: 10.1593/neo.91298.
9
Influence of hepatitis B virus X and core promoter mutations on hepatocellular carcinoma among patients infected with subgenotype C2.乙型肝炎病毒X和核心启动子突变对C2亚基因型感染患者肝细胞癌的影响
J Clin Microbiol. 2007 Oct;45(10):3191-7. doi: 10.1128/JCM.00411-07. Epub 2007 Jul 25.
10
Nucleotide change of codon 38 in the X gene of hepatitis B virus genotype C is associated with an increased risk of hepatocellular carcinoma.乙型肝炎病毒C基因型X基因中第38密码子的核苷酸变化与肝细胞癌风险增加相关。
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中国东部地区肝细胞癌组织与癌旁肝组织中乙肝病毒X基因变异的鉴定

Identification of hepatitis B virus X gene variants between hepatocellular carcinoma tissues and pericarcinoma liver tissues in Eastern China.

作者信息

Wang Dan, Cai Hao, Yu Wen-Bo, Yu Long

机构信息

The State Key Laboratory of Genetics Engineering, Fudan University Shanghai, 200433, P.R. China.

出版信息

Int J Clin Exp Pathol. 2014 Aug 15;7(9):5988-96. eCollection 2014.

PMID:25337243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4203214/
Abstract

UNLABELLED

Hepatocellular carcinoma (HCC) is one of the most malignant tumors worldwide, especially in Eastern China where HBV infection confirmed as the most important pathological element. HBV X gene, extremely easy to mutate and integrate into hepatocytes, plays a significant role in HBV infection and HCC development. We deduced that mutations of integrated HBx gene make transformation more malignant. The aim of the study was to investigate whether there were different mutation patterns between the HCC tissues and the pericarcinoma liver tissues (PCLT) from patients with HCC in Eastern China.

METHODS

HBx genes extracted from 287 HCC tissue samples and 195 PCLT tissue samples were analyzed by sequence alignment and stratified analysis with the matched medical records.

RESULTS

Mutations occurred complicated and changeable in both HCC and PCLT. COOH-terminal truncation is more frequently found in HCC than PCLT (P < 0.05). There is no single site mutation of nucleic acid or amino acid makes distribution discrepancy between HCC and PCLT. Hydrophobic/hydrophilic character of amino acid of site 43, 47, 127, 131, 132 make distribution discrepancy between HCC and PCLT in men when stratified for gender (P < 0.05). Hydrophobic/hydrophilic character of amino acid of site 40 makes distribution discrepancy between HCC and PCLT in both male and female (P < 0.05). Hydrophobic/hydrophilic character of amino acid of site 47 and 127 make significant discrepancy among clinical stage I, II, III (P < 0.05).

CONCLUSIONS

During the infection and replication of HBV, HBx mutates to adjust itself to the hepatocyte and increase the carcinogenesis. COOH-terminal truncated HBX may play a stimulative role in HBV-related HCC carcinogenesis as well as hydrophobic/hydrophilic character changes in some specific amino acid sites.

摘要

未标记

肝细胞癌(HCC)是全球最恶性的肿瘤之一,尤其是在中国东部地区,乙肝病毒(HBV)感染被确认为最重要的病理因素。HBV X基因极易发生突变并整合到肝细胞中,在HBV感染和HCC发展中起重要作用。我们推测整合的HBx基因突变会使转化更具恶性。本研究的目的是调查中国东部HCC患者的HCC组织与癌旁肝组织(PCLT)之间是否存在不同的突变模式。

方法

从287份HCC组织样本和195份PCLT组织样本中提取的HBx基因,通过序列比对和与匹配病历的分层分析进行分析。

结果

HCC和PCLT中的突变发生复杂且多变。COOH末端截短在HCC中比在PCLT中更常见(P < 0.05)。没有单个核酸或氨基酸位点突变使HCC和PCLT之间的分布存在差异。当按性别分层时,第43、47、127、131、132位点氨基酸的疏水/亲水性特征使男性的HCC和PCLT之间存在分布差异(P < 0.05)。第40位点氨基酸的疏水/亲水性特征使男性和女性的HCC和PCLT之间存在分布差异(P < 0.05)。第47和127位点氨基酸的疏水/亲水性特征在临床I、II、III期之间存在显著差异(P < 0.05)。

结论

在HBV感染和复制过程中,HBx发生突变以适应肝细胞并增加致癌作用。COOH末端截短的HBX可能在HBV相关HCC致癌过程中起促进作用,以及某些特定氨基酸位点的疏水/亲水性特征变化。