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| 1 | Factors predicting occurrence and prognosis of hepatitis-B-virus-related hepatocellular carcinoma显示文摘Primary liver cancer is an important cause of cancer death,and hepatocellular carcinoma(HCC) accounts for 70%-85% of total liver cancer worldwide.Chronic hepatitis B virus(HBV) infection contributes to > 75% of HCC cases.High serum viral load is the most reliable indicator of viral replication in predicting development of HCC.HBV genotype C is closely associated with HCC in cirrhotic patients aged > 50 years,whereas genotype B is associated with development of HCC in non-cirrhotic young patients and postoperative relapse of HCC.Different HBV subgenotypes have distinct patterns of mutations,which are clearly associated with increased risk of HCC.Mutations accumulate during chronic HBV infection and predict occurrence of HCC.Chronic inflammation leads to increased frequency of viral mutation via cellular cytidine deaminase induction.Mutations are negatively selected by host immunity,whereas some immuno-escaped HBV mutants are active in hepatocarcinogenesis.Inflammatory pathways contribute to the inflammation-necrosis-regeneration process,ultimately HCC.Their hallmark molecules can predict malignancy in HBV-infected subjects.Continuing inflammation is involved in hepatocarcinogenesis and closely related to recurrence and metastasis.HBV load,genotype C,viral mutations and expression of inflammatory molecules in HBV-related HCC tissues are significantly associated with poor prognosis.Imbalance between intratumoral CD8+ T cells and regulatory T cells or Th1 and Th2 cytokines in peritumoral tissues can predict prognosis of HBV-related HCC.These factors are important for developing active prevention and surveillance of HBV-infected subjects who are more likely to develop HCC,or for tailoring suitable treatment to improve survival or postpone postoperative recurrence of HCC. | Yi-Fang Han Jun Zhao Li-Ye Ma Jian-Hua Yin Wen-Jun Chang Hong-Wei Zhang Guang-Wen Cao | 2011 | World Journal of Gastroenterology2011，17，38： | 54 |
| 2 | Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats显示文摘BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC. | Dong, Zhi-Zhen Yao, Deng-Fu Wu, Wei Yao, Min Yu, Hong-Bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，2： | 31 |
| 3 | Molecular characteristics and stages of chronic hepatitis B virus infection显示文摘Hepatitis B virus (HBV) is a common viral pathogen that causes a substantial health burden worldwide. Remarkable progress has been made in our understanding of the natural stages of chronic HBV infection. A dynamic balance between viral replication and host immune response is pivotal to the pathogenesis of liver disease. Knowledge of the HBV genome organization and replication cycle can unravel HBV genotypes and molecular variants, which contribute to the heterogeneity in outcome of chronic HBV infection. Most HBV infections are spontaneously resolved in immunocompetent adults, whereas they become chronic in most neonates and infants at a great risk of developing complications such as cirrhosis and hepatocellular carcinoma (HCC). Those with chronic HBV infection may present in one of the four phases of infection: immune tolerance, immune clearance [hepatitis B eantigen (HBeAg)-positive chronic hepatitis B (CHB)], inactive carrier state, and reactivation (HBeAg-negative CHB). Understanding the dynamic nature of chronic HBV infection is crucial in the management of HBV carriers. Long-term monitoring and optimal timing of antiviral therapy for chronic HBV infection help to prevent progression of HBV-related liver disease to its later stage, particularly in patients with higher risk markers of HCC, such as serum DNA concentration, HBeAg status, serum aminotransferase, HBV genotypes, and pre-core or core mutants. | Ying-Hui Shi Chang-He Shi | 2009 | World Journal of Gastroenterology2009，15，25： | 32 |
| 4 | Hepatitis B virus,HBx mutants and their role in hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC)is one of the leading causes of death induced by cancer in the modern world and majority of the cases are related to chronic hepatitis B virus(HBV)infection.HBV-encoded X protein(HBx)is known to play a pivotal role in the pathogenesis of viral induced HCC.HBx is a multifunctional protein of17 kDa which modulates several cellular processes by direct or indirect interaction with a repertoire of host factors resulting in HCC.HBX might interfere with several cellular processes such as oxidative stress,DNA repair,signal transduction,transcription,protein degradation,cell cycle progression and apoptosis.A number of reports have indicated that HBx is one of the most common viral ORFs that is often integrated into the host genome and its sequence variants play a crucial role in HCC.By mutational or deletion analysis it was shown that carboxy terminal of HBx has a likely role in protein-protein interactions,transcriptional transactivation,DNA repair,cell,signaling and pathogenesis of HCC.The accumulated evidence thus far suggests that it is difficult to understand the mechanistic nature of HBx associated HCC,and HBx mediated transcriptional transactivation and signaling pathways may be a major determinant.This article addresses the role of HBx in the development of HCC with particular emphasis on HBx mutants and their putative targets. | Ashraf Ali Hany Abdel-Hafiz Mohd Suhail Amany Al-Mars Mohammad Khalid Zakaria Kaneez Fatima Sultan Ahmad Esam Azhar Adeel Chaudhary Ishtiaq Qadri | 2014 | World Journal of Gastroenterology2014，20，30： | 29 |
| 5 | Recent advances in hepatitis B virus research:A German point of view显示文摘More than 30 years after the discovery of human hepatitis B virus (HBV) this virus remains to be one of the major global health problems. In infected adolescents or adults, 5%-10% will lead to a chronic carrier state, whereas in infected neonates up to 90% develop chronicity. It is estimated that about 370 million people are chronic carriers of HBV worldwide. In many regions of the world, chronic HBV infection is still the major cause of liver cirrhosis and hepatocellular carcinoma. During the last 30 years, many steps of the viral life cycle have been unravelled, mainly due to cloning, sequencing and expression of the genomic DNA extracted from HBV virions. This has lead to the development of a safe and efficient vaccine and sensitive tests for HBV surface protein (HBsAg) allowing reliable diagnosis and screening of blood products. More recently, a growing number of reverse transcriptase inhibitors have been developed. However, together with these improvements new deficiencies in prevention and cure of HBV infections are becoming apparent. Although HBV is a DNA virus, it is highly variable under immunity or drug induced selection pressure, resulting in vaccine-related escape mutants and drug resistance. To overcome these challenging problems new antivirals and optimised vaccines have to be developed. | Dieter Glebe | 2007 | World Journal of Gastroenterology2007，13，1： | 25 |
| 6 | Tumor initiation and progression in hepatocellular carcinoma: risk factors, classification, and therapeutic targets显示文摘Hepatocellular 癌(HCC ) 每年是为 500 000 死亡负责的世界范围的一个主要健康问题。很多个风险因素与也被联系疾病或它的前进的正式就职;这些与肝炎 B 或 C 病毒,白酒消费,非酒精的 steatohepatitis 和某些先天的混乱包括感染。在约 80% 盒子, HCC 与肝硬化或先进纤维变性并且与发炎和氧化应力被联系。在这评论,我们为 HCC 第一集中于不同风险因素并且总结由哪个各被认为贡献 HCC 的机制。在第二部分,我们看涉及癌症前进的分子的过程。HCC 开发作为 multistep 进程被认出通常在许多年发展。在几个变化在房间和那积累的这个时期上刺激诽谤转变,生长,和变形行为。在最近的年,不仅肿瘤房间本身而且肿瘤 microenviroment 在一个肿瘤的发展起一个主要作用,变得明显。与这 microenviroment 在发炎和肝硬化的角色之间有一个直接连接。在 vitro 并且在 vivo,它被看了那肿瘤形成,变形性质被连接到上皮间充质的转变(EMT ) ,由 facillitates,肿瘤房间是尝试移居到更赞成的 microenviroment 的一个过程。几个组由 microarray 在 HCC 和它的包围织物分析了基因表示,这导致了分子的分类进班的一个不同数字。这里,我们也发现为组织缺氧的一个角色导致了基因表示导致一临床上在 HCC 的更好攻击的基因表示。分子的分析也帮助识别重要细胞的小径和可能的治疗学的目标。这样为肝癌症显示出临床的申请的第一个分子是 multikinase 禁止者 sorafenib,其它当前在象 mTOR 禁止者 everolimus 一样的临床的研究的不同阶段。 | Tamara SEVERI Hannah van MALENSTEIN Chris VERSLYPE Jos F van PELT | 2010 | Acta Pharmacologica Sinica2010，31，11： | 23 |
| 7 | 慢性乙肝病毒感染患者血清免疫调节因子检测及基因多态性分析显示文摘目的检测不同人群血清免疫调节因子水平,为临床检测和治疗慢性乙肝病毒感染提供依据。方法 2013年6月-2016年6月广东省南方医科大学珠江医院诊治的慢性HBV感染患者116例。按HBV感染后临床表现分为:慢性HBV携带组22例,慢性乙型肝炎组39例和乙型肝炎肝硬化组55例。对照组选取健康体检者29例。采集受检者静脉血,分离血清,采用ELISA检测HBsAg、HBeAg、抗HBs和抗HCV等,采用双抗体夹心ABC-ELISA法检测IFN-γ、IL-4及IL-12等细胞因子,采用全自动生化仪检测肝功能指标。采用聚乙二醇沉淀法浓缩血清中的HBV。碱变形法提取血DNA,采用PCR热扩增HBV DNA。提取人全血DNA,采用PCR热扩增TNF-α-857和TNF-α-863并进行酶切和基因多态性分析。结果 HBV携带组、慢性乙型肝炎组、肝硬化组和对照组的ALB(g/L)分别为:38.78±9.56、23.8±8.2、23.6±6.4和47.43±9.56,组间比较差异有统计学意义(P<0.05);ALT(U/L)浓度分别为:98.5±32.8、187.7±37.1、102.6±41.9和32.1±11.8,组间比较差异有统计学意义(P<0.05);TBIL(μmol/L)分别为:68.72±32.51、72.2±47.86、73.6±42.9和15.39±5.33,组间比较差异有统计学意义(P<0.05);IL-4(pg/ml)分别为:108.71±31.52、96.89±26.29、92.74±28.47和28.43±5.56,组间比较差异有统计学意义(P<0.05);IL-12(pg/ml)分别为:33.96±7.38、58.31±10.12、43.29±9.53和17.45±7.82,组间比较差异有统计学意义(P<0.05)。IFN-γ(pg/ml)分别为:48.65±11.57、73.51±20.82、56.31±42.9和22.71±5.39,组间比较差异有统计学意义(P<0.05)。TNF-α-857基因多态性检测HBV携带组CC纯合型15例,TT纯合型1例,CT杂合型6例;慢性乙型肝炎组CC纯合型26例,TT纯合型3例,CT杂合型10例;肝硬化组CC纯合型36例,TT纯合型4例,CT杂合型15例;对照组CC纯合型15例,TT纯合型3例,CT杂合型11例。TNF-α-863基因多态性检测,HBV携带组CC纯合型14例,AA纯合型2例,CA杂合型6例;慢性乙型肝炎组CC纯合型24例,AA纯合型3例,CA杂合型12例;肝硬化组CC纯合型31例,AA纯合型3例,CA杂合型21例;对照组CC纯合型20例,AA纯合型1例,CA杂合型7例。结论血清ALB、ALT、TBIL、IL-4、IL-12和IFN-γ浓度检测能够反映慢性乙肝病毒感染者肝功能损伤程度,组织中TNF-α基因的多态性对疾病发展和预测提供了可能性。 | 连桂秀 毛华 卢敏 靳丹丹 | 2019 | 中国病原生物学杂志2019，14，9： | 15 |
| 8 | Establishment and primary application of a mouse model with hepatitis B virus replication显示文摘瞄准:与肝炎 B (HBV ) 复制建立一个快速、方便的动物模型。方法:HBV-replication-competent 原生质标志的一个裸体 DNA 解决方案经由尾巴静脉被转移到 BALB/C 鼠标,用一个水动力学在活体内 transfection 过程。在注射以后,这些老鼠在 d 上被牺牲 1, 3, 4, 5, 7 和 10。在肝的 HBV DNA 复制中介被南部的污点杂交分析。肝炎 B 核心抗原(HBcAg ) 和在肝的肝炎 B 表面抗原(HBsAg ) 的表示被免疫组织化学检查。浆液 HBsAg 和肝炎 B e 抗原(HBeAg ) 被连接酶的免疫吸着剂试金(ELISA ) 检测。HBV 复制的抑制在与 polyinosinic-polytidylin 酸(polyIC ) intraperitoneally 对待的 HBV 复制模型老鼠被比较或缓冲磷酸盐 saline (PBS ) 。结果:在水动力学在活体内 transfection 以后,在老鼠肝的 HBV DNA 复制中介在 d 上是可检测的 1 并且在 d 上丰富 3 和 4,层次稍微被减少并且在 d 之间仍然保持相对稳定 5 和 7,并且在 d 上是几乎无法发现的 10。HBcAg 和 HBsAg 的表示模式类似于 HBV 复制中介 DNA 的,除了他们在 d 上到达了一座山峰之外 1 在注射以后。在 HBV DNA 复制中介的明显的差别都没在肝的左、正确、中间的脑叶被观察。有 polyIC 的术后疗法,在肝的 HBV 中间的 DNA 的水平在与 PBS 注射的控制老鼠是比那低的。结论:有 HBV 复制的高水平的一个快速、方便的老鼠模型被开发并且过去常在 HBV 复制上调查 polyIC 的禁止的效果,它为未来提供一个有用工具 HBV 染色体的功能的研究。 | Feng-Jun Liu Li Liu Fang He Su Wang Tao-You Zhou Cong Liu Lin-Yu Deng Hong Tang | 2007 | World Journal of Gastroenterology2007，13，40： | 13 |
| 9 | Core promoter: A critical region where the hepatitis B virus makes decisions显示文摘The core promoter(CP)of the viral genome plays an important role for hepatitis B virus(HBV)replication as it directs initiation of transcription for the synthesis of both the precore and pregenomic(pg)RNAs.The CP consists of the upper regulatory region and the basal core promoter(BCP).The CP overlaps with the 3’-end of the X open reading frames and the 5’-end of the precore region,and contains cis-acting elements that can independently direct transcription of the precore mRNA and pgRNA.Its transcription regulation is under strict control of viral and cellular factors.Even though this regulatory region exhibits high sequence conservation,when variations appear,they may contribute to the persistence of HBV within the host,leading to chronic infection and cirrhosis,and eventually,hepatocellular carcinoma.Among CP sequence variations,those occurring at BCP may dysregulate viral gene expression with emphasis in the hepatitis B e antigen,and contribute to disease progression.In this review these molecular aspects and pathologic topics of core promoter are deeply evaluated. | Jorge Quarleri | 2014 | World Journal of Gastroenterology2014，20，2： | 13 |
| 10 | Characteristics of hepatic nuclear-transcription factor-kappa B expression and quantitative analysis in rat hepatocarcinogenesis显示文摘BACKGROUND:Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.We analyzed the expression of nuclear-transcription factor-kappa B(NF-κB) during hepatocarcinogenesis in order to evaluate its dynamic expression and its clinical value in the development and diagnosis of HCC. METHODS:Hepatoma models were induced by oral administration of 2-acetamidoflurene(2-FAA)to male Sprague-Dawley rats.Morphological changes were observed after hematoxylin and eosin staining.The cellular distribution of NF-κB expression during different stages of cancer development was investigated by immunohistochemistry, and the level of NF-κB expression in liver tissues was quantitatively analyzed by ELISA.The gene fragments of hepatic NF-κB were amplified by nested-polymerase chain reaction assay. RESULTS:Hepatocytes showed vacuole-like degeneration during the early stages,then had a hyperplastic nodal appearance during the middle stages,and finally progressed to tubercles of cancerous nests with high differentiation. The NF-κB-positive material was buff-colored,fine particles localized in the nucleus,and the incidence of NF-κB-positive cells was 81.8%in degeneration,83.3%in precancerous lesions,and 100%in cancerous tissues.All of these values were higher than those in controls(P<0.01). Hepatic NF-κB expression and hepatic NF-κB-mRNA were also higher during the course of HCC development(P<0.01).CONCLUSION:The NF-κB signal transduction pathway is activated during the early stages of HCC development, and its abnormal expression may be associated with the occurrence of HCC. | Wu, Wei Yao, Deng-Fu Qiu, Li-Wei Sai, Wen-Li Shen, Jun-Jun Yu, Hong-Bo Wu, Xin-Hua Li, Yue-Ming Wang, Yi-Lang Gu, Wen-Jing | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，5： | 12 |
| 11 | Prevention of hepatocellular carcinoma in patients with chronic hepatitis B显示文摘Patients with chronic hepatitis B are at significant risk for hepatocellular carcinoma(HCC). Globally,over half a million people each year are diagnosed with HCC,with marked geographical variations. Despite overwhelming evidence for a causal role of hepatitis B virus(HBV) infection in the development of HCC and a well-established relationship between high baseline hepatitis B viral load and cumulative risk of HCC,the molecular basis for this association has not been fully elucidated. In addition,a beneficial role for antiviral therapy in preventing the development of HCC has been difficult to establish. This review examines the biological and molecular mechanisms of HBV-related hepatocarcinogenesis,recent results on the effect of modern nucleos(t)ides on the rate of HCC development in high risk HBV cohorts and the potential mechanisms by which long-term antiviral therapy with potent inhibitors of HBV replication might reduce the risk of HCC in patients with chronic hepatitis B. Although evidence from randomized controlled trials shows the favourable effects of antiviral agentsin achieving profound and durable suppression of HBV DNA levels while improving liver function and histology,robust evidence of other long-term clinical outcomes,such as prevention of HCC,are limited. | Conrado M Fernández-Rodríguez María Luisa Gutiérrez-García | 2014 | World Journal of Gastrointestinal Pharmacology and Therapeutics2014，5，3： | 9 |
| 12 | 小肝癌的临床诊断与个体化治疗显示文摘目的探讨小肝癌的临床诊断与个体化治疗方案。方法回顾性分析2007年1月至2009年1月在东莞市人民医院治疗的53例小肝癌患者的临床资料,总结小肝癌患者个体化诊治的经验。结果 53例中手术切除35例,其中肿瘤位置较深而术中无法扪及18例,15例联合B超定位,3例术中体内标志联合CT/MRI定位。2例手术切除者因上消化道大出血及肝功能衰竭于术后2个月内死亡。微创治疗18例,其中射频消融术(RFA)13例,无水酒精注射术(PEI)3例,肝动脉化疗栓塞术(TA-CE)2例。手术切除组和微创治疗组3年生存率分别为75.2%和71.3%;1、2、3年复发率分别为13.3%、24.5%、37.1%和17.4%、31.8%、41.6%,差异均无统计学意义(均P>0.05)。结论小肝癌的早期诊断应注意乙肝病史,同时结合多种检查及密切随访综合判断。术中B超和体内标志联合CT/MRI能准确定位微小病灶。小肝癌的治疗应制定个体化的治疗方案。 | 胡夏荣 俞武生 卢春丽 吴志明 卢焕全 尹永硕 黄兆伦 叶镇彭 王在国 | 2013 | 中国肿瘤外科杂志2013，5，2： | 6 |
| 13 | 与乙肝病毒蛋白相互作用的宿主因子研究进展显示文摘乙型肝炎病毒(Hepatitis B virus,HBV)是引起肝炎疾病的主要因素。HBV自身基因组极其简单,病毒复制生命过程都是在宿主因子协同作用下完成的。这些协同作用包括病毒包膜蛋白的加工对伴侣的依赖性、细胞因子对核衣壳的动力学修饰和转运、伴侣分子引发的反转录过程、宿主多泡体通路组分促进病毒粒子成熟与分泌以及X蛋白调控机制。本文综述了宿主因子对HBV以上几方面的影响最新研究进展,旨在为新型乙肝药物设计提供基础。 | 尧晨光 魏艳红 寇铮 胡康洪 | 2015 | 中国病原生物学杂志2015，10，10： | 6 |
| 14 | 乙肝病毒X蛋白对人肝细胞内β-catenin定位及转录活性的影响显示文摘目的研究HBx对Wnt/Wingless信号传导通路中主要信号分子β-catenin的影响,探讨HBV相关性HCC的发生机制。方法Ad-HBx转染人肝细胞系L02细胞,免疫细胞化学和Luciferase检测细胞中β-catenin细胞定位及活性变化。结果免疫细胞化学:转染重组HBx腺病毒前L02细胞中β-catenin仅在细胞质有少量表达,转染后胞质表达明显增强,并出现胞核的大量积聚;Luciferase检测:实验组TOP荧光素酶活性与对照组及空白组相比明显增强,为阴性对照的11倍(P<0.05),Ad-HBx感染后24 h和36 h的TOP荧光素酶活性无显著差异。结论Ad-HBx重组腺病毒在体外能有效转染人肝细胞系L02细胞,受感染细胞能有效表达HBx蛋白,HBx影响了人肝细胞系L02细胞中β-catenin的细胞定位及转录活性。 | 丁浩 何柳兴 冯涛 | 2009 | 基础医学与临床2009，29，5： | 5 |
| 15 | HBx基因缺失突变体HBx-d382对L02细胞增殖及非锚定依赖生长能力的影响显示文摘目的:建立稳定表达HBx基因缺失突变体(HBx-d382)的L02肝细胞株,并探讨其对L02细胞增殖的影响.方法:含HBx-d382重组质粒(pcDNA3.0/HBx-d382)经过PCR扩增、双酶切及测序鉴定后,通过脂质体转染和G418筛选获得稳定表达HBx-d382的L02肝细胞株.PCR鉴定基因组中HBx-d382基因整合.RT-PCR和Westernblot鉴定其表达,进一步通过MTT法,软琼脂克隆形成实验检测HBx-d382对L02细胞增殖及非锚定依赖生长能力的影响.用流式细胞仪检测其对细胞周期的影响.结果:经PCR扩增、双酶切及测序鉴定HBx-d382重组质粒构建正确.稳定转染该质粒的L02细胞基因组存在HBx-d382整合.RT-PCR及Westernblot表明在RNA水平和蛋白水平存在HBx-d382表达,稳定表达HBx-d382的L02细胞其增殖能力和非锚定生长能力增强,S+G2期细胞比例升高.结论:成功构建了HBx缺失突变体的真核表达模型,证实HBx缺失突变体能影响细胞增殖,这种效应可能与其影响细胞周期调控相关. | 胡志亮 谭德明 侯周华 谢萍 刘国珍 欧阳奕 刘菲 刘洪波 | 2010 | 世界华人消化杂志2010，18，11： | 5 |
| 16 | 高尔基体糖蛋白-73异常表达与肝癌诊断显示文摘高尔基体糖蛋白-73(GP73)为经糖基化修饰的膜蛋白,肝癌患者中GP73上调表达。外周血中较高水平的GP73与肝癌相关,在肝癌早期诊断方面,GP73优于AFP,是一具有较高临床诊断价值的新的肝癌标志物。 | 赛文莉 姚登福 | 2011 | 胃肠病学和肝病学杂志2011，20，1： | 4 |
| 17 | Expression of B7-H4 and hepatitis B virus X in hepatitis B virus-related hepatocellular carcinoma显示文摘AIM: To investigate the expression and clinical significance of B7-H4 and hepatitis B virus X(HBx) protein in hepatitis B virus-related hepatocellular carcinoma(HBV-HCC).METHODS: The expression of B7-H4 in the human HCC cell lines Hep G2 and Hep G2.2.15 were detected by western blot, flow cytometry, and immunofluorescence. The expression of B7-H4 and HBx in 83 HBV-HCC was detected by immunohistochemistry, and the relationship with clinicopathological features was analyzed. Paraffin sections were generated from 83 HBV-HCC patients(22 females and 61 males) enrolled in this study. The age of these patients ranged from 35 to 77 years, with an average of 52.5 ± 11.3 years. All experiments were approved by the Ethics Committees of the Second Affiliated Hospital, Zhejiang University School of Medicine.RESULTS: B7-H4 was significantly upregulated in Hep G2.2.15 cells compared to Hep G2 cells. Specifically, the protein expression of B7-H4 in the lysates of Hep G2 cells was more than that in Hep G2.2.15 cells. In addition, HBx was expressed only in Hep G2.2.15 cells. Similar data were obtained by flow cytometry. The positive rates of B7-H4 and HBx in the tissues of 83 HBV-HCC patients were 68.67%(57/83) and 59.04%(49/83), respectively. The expression of HBx was correlated with tumor node metastases(TNM) stage, and the expression of B7-H4 was positively correlated with HBx(rs = 0.388; p < 0.01). The expression level of B7-H4 in HBx-positive HBV-HCC tissues was substantially higher than that in HBx-negative HBV-HCC tissues. The expression level of B7H4 was negatively related to tumor TNM stage.CONCLUSION: Higher expression of HBx and B7-H4 was correlated with tumor progression of HBV-HCC, suggesting that B7-H4 may be involved in facilitating HBV-related hepatocarcinogenesis. | Bo Hong Yun Qian Hong Zhang Yi-wen Sang Lin-fang Cheng Qi wang Song Gao Min Zheng Hang-ping Yao | 2016 | World Journal of Gastroenterology2016，22，18： | 4 |
| 18 | 外周血高尔基体糖蛋白-73表达水平对肝细胞癌的诊断与鉴别诊断价值显示文摘目的定量分析肝病患者血清高尔基体糖蛋白-73(GP73)水平,探讨其对肝细胞肝癌(HCC)的诊断与鉴别诊断价值。方法收集不同肝病患者外周血标本,以酶联免疫吸附法(ELISA)检测GP73浓度,并分析与甲胎蛋白(AFP)的相互关系。结果血GP73表达水平,正常对照组为(28.83±21.00)ng/ml,慢性肝炎组为(49.86±40.46)ng/ml,肝硬化组为(62.30±56.30)ng/ml,肝癌组为(66.75±69.97)ng/ml;GP73水平随着肝病的进展呈进行性增加,肝癌组明显高于对照组和慢性肝炎及肝硬化组(P<0.05)。肝癌患者血GP73表达水平在HBV感染(HBsAg阳性/阴性)、肝外转移与否组间对比,差异有统计学意义(P<0.05)。且GP73与AFP表达改变呈显著正相关(r=0.961,P=0.039),血AFP的ROC曲线下面积为0.877,GP73为0.931,GP73与AFP联合检测对肝癌有互补诊断价值。结论血GP73表达异常与肝癌发展密切相关,定量检测有助于肝癌的诊断和鉴别。 | 赛文莉 姚登福 吴玮 邱历伟 杨君伶 张海健 蔚丹丹 秦呈林 | 2011 | 中华临床医师杂志(电子版)2011，5，24： | 4 |
| 19 | 肝细胞肝癌发病过程中HBVx及COX-2的作用显示文摘目的研究HBVx和COX-2在肝细胞肝癌发病过程中的作用。方法145例HCC、78例肝炎后肝硬化及16例来自尸检的正常肝组织标本经病理复查后制成组织芯片,进行HE及免疫组织化学染色,评定各指标的染色指数。结果HCC组HB-Vx平均阳性表达指数高于肝硬化组(P<0.01)。HBVx在高、中、低分化HCC组间表达差异有统计学意义。COX-2免疫组化染色在肝硬化组表达较强;在HCC组和正常人肝细胞胞质中表达较弱。HCC组肿瘤细胞胞质中COX-2阳性表达指数低于肝硬化组(P<0.01)。COX-2在高、中、低HCC组间表达差异有统计学意义。相关性分析表明145例HCC中HBVx表达与COX-2表达存在正相关(P=0.000)。结论HBVx可通过调节COX-2的表达参与HCC发病过程。 | 赵秀兰 郄硕 赵学铭 焦振山 张诗武 古强 王星辉 赵楠 姚智 | 2008 | 临床与实验病理学杂志2008，24，3： | 4 |
| 20 | HBV准种与肝细胞癌发生发展关系的研究进展显示文摘乙型肝炎病毒(hepatitis B virus,HBV)为一嗜肝细胞性DNA病毒,具有复制率高、突变率高的特点,在宿主体内以准种形式存在。HBV感染不仅可以引起隐匿性、急性和慢性病毒性肝炎,还与肝硬化和肝细胞癌(hepatocellular carcinoma,HCC)的发生发展密切相关。关注HBV准种的研究,有助于从整体和动态的角度认识HBV基因突变的特点、规律及其生物学特性,进而探究HBV准种与HCC发生、发展的关系,为早期预防、早期诊断和合理治疗提供新策略。本文就HBV准种与HCC发生发展的关系作一综述。 | 任静静 邓伟 | 2016 | 中国癌症防治杂志2016，8，4： | 4 |
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