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| 1 | COOH-terminal deletion of HBx gene is a frequent event in HBV-associated hepatocellular carcinoma显示文摘AIM:To investigate the hepatitis B virus (HBV) x gene (HBx) state in the tissues of HBV-related hepatocellular carcinoma (HCC) in Chinese patients and whether there were particular HBx mutations. METHODS: HBx gene was amplified and direct sequencing was used in genomic DNA samples from 20 HCC and corresponding non-cancerous liver tissues from HBsAg-positive patients. HBV DNA integration and HBx deleted mutation were validated in 45 HCC patients at different stages by Southern blot analysis and polymerase chain reaction methods. RESULTS: The frequencies of HBx point mutations were significantly lower in HCC than their corresponding non- cancerous liver tissues (11/19 vs 18/19, P = 0.019). In contrast, deletions in HBx gene were significantly higher in HCC than their non-cancerous liver tissues (16/19 vs 4/19, P < 0.001). The deletion of HBx COOH-terminal was detected in 14 HCC tissues. A specific integration of HBx at 17p13 locus was also found in 8 of 16 HCC, and all of them also exhibited full-length HBx deletions. Integrated or integrated coexistence with replicated pattern was obtained in 45.5% (20/45) - 56.8% (25/45) tumors and 40.9% (18/45) - 52.3% (23/45) non-tumor tissues. CONCLUSION: HBx deletion, especially the COOH- terminal deletion of HBx is a frequent event in HBV-associated HCC tissues in China. HBV integration had also taken place in partial HCC tissues. This supporting the hypothesis that deletion and probably integrated forms of the HBx gene may be implicated in liver carcinogenesis. | Xiao-Hong Liu Jing Lin Shu-Hui Zhang Shun-Min Zhang Mark A Feitelson Heng-Jun Gao Ming-Hua Zhu | 2008 | World Journal of Gastroenterology2008，14，9： | 24 |
| 2 | Oxidative stress and antioxidants in hepatic pathogenesis显示文摘Long term hepatitis B virus (HBV) infection is a major risk factor in pathogenesis of chronic liver diseases,including hepatocellular carcinoma (HCC). The HBV encod-ed proteins,hepatitis B virus X protein and preS,appear to contribute importantly to the pathogenesis of HCC. Both are associated with oxidative stress,which can damage cellular molecules like lipids,proteins,and DNA during chronic infection. Chronic alcohol use is another important factor that contributes to oxidative stress in the liver. Previous studies reported that treatment with antioxidants,such as curcumin,silymarin,green tea,and vitamins C and E,can protect DNA from damage and regulate liver pathogenesis-related cascades by reducing reactive oxygen species. This review summarizes some of the relationships between oxidative stress and liver pathogenesis,focusing upon HBV and alcohol,and suggests antioxidant therapeutic approaches. | Hye-Lin Ha Hye-Jun Shin Mark A Feitelson Dae-Yeul Yu | 2010 | World Journal of Gastroenterology2010，16，48： | 18 |
| 3 | Differentially expressed genes in hepatocellular carcinoma induced by woodchuck hepatitis B virus in mice显示文摘INTRODUCTIONHepatocellular carcinoma(HCC)is one of the major causes of death in the word.The mechanism of carcinogenesis is unknown,although it is widely accepted that HBV and HCV are clsely related to liver cancer[1-5[1-5].Previously,a variety of studies have described the differences in gene expression which distinguished tumor from nontumor[6-11].Cloning of the genes,especially the genes associated with HBV and HCV,is still very important to account for the development of liver cancer. | Mark Feitelson | 2001 | World Journal of Gastroenterology2001，7，4： | 11 |
| 4 | 乙型肝炎病毒X抗原转导细胞差示表达全长基因C2的克隆及初步功能研究显示文摘目的 克隆乙型肝炎病毒X抗原 (HBxAg)相关肝癌差示表达基因并做功能研究。方法 (1)用逆转录病毒方法建立表达HBxAg细胞模型。 (2 )用抑制差减杂交做基因差示表达分析。 (3)做RNA印迹分析 (NorthernBlot)及原位分子杂交筛选基因探针。 (4 )用 5′和 3′迅速末端扩增法 (RACEPCR)进行全长基因序列扩增 ,并进行体外蛋白翻译及制备抗体 ,做蛋白质印迹 (WesternBlot)分析。(5 )进行该基因细胞内转导 ,进行功能研究。结果 共得到 10个cDNA探针 ,其中 8个因HBX表达上调 ,2个表达下降。经筛选及全长基因扩增 ,得到 1个全长为 1.35kb、编码 113个氨基酸的全长基因C2 ,和蛋白翻译起始因子 (Suil)同源 ,其表达被HBX抑制。初步功能研究显示 ,此基因对细胞生长具有抑制作用 ,并且正常肝组织中其mRNA信号明显高于肝癌组织。结论 我们不仅克隆出HBX相关基因C2并进行了功能研究 ,还首次提出DNA病毒 (HBV) | 刘杰 连兆瑞 潘静波 胡家露 朱明华 窦科峰 丁杰 吴开春 樊代明 Mark Feitelson | 2000 | 中华医学杂志2000，80，6： | 11 |
| 5 | Cloning of differentially expressed genes in human hepatocellular carcinoma and nontumor liver显示文摘INTRODUCTIONThe mechanism of hepatocellular carcinoma(HCC)is still unclear,although some genes have been found to play a role in the transformation of liver cells,and a variety of studies have described differences in gene expression which distinguished tumor from nontumor[1-6].The new genes,especially the functional genes directly related with tumor are still worth being found.The purpose of our study is to find the different genes between human liver tumor and normal tissues using suppression subtractive hybridization. | Xiao-Yan Cao Jie Liu Zhao-Rui Lian Marcy Clayton Jia-Lu Hu Ming-Hua Zh Dai-Ming Fan Mark Feitelson Institute of Digestive Diseases,Xijing Hospital,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,ChinaDepartment of Pathology & Cell Biology,Thomas Jefferson University,Philadelphia,PA19107 USADepartment of Pathology,Second Military Medical University,Shanghai 200433,China | 2001 | World Journal of Gastroenterology2001，7，4： | 7 |
| 6 | ELISA方法检测肝癌血清标志物的应用显示文摘目的对已建立的肝癌血清标志物ELISA检测方法进行扩大规模临床样本检测,进一步评价和优化该方法。方法利用本实验室建立的肝癌血清标志物ELISA检测方法,对407份肝病患者血清和95份正常献血员血清进行检测,并对检测结果进行分析。结果324份HBV感染后的肝癌、肝硬化及肝炎患者血清样本中,2种或2种以上指标阳性比例分别为77.6%、76.1%和52.5%,肝癌患者3种或3种以上指标阳性比例较肝硬化和肝炎患者分别高39.9%和310%;在正常献血员、药物性肝炎、酒精性肝炎及其他类型的癌症患者中,87.5%~100%的患者肝癌血清标志物分子≤1种;URG7是最早出现的抗体阳性标志物分子,URG11和S15a抗体则在进展后期或已发展为肝癌的患者血清中呈优势比例出现。结论5种肝癌血清标志物分子与肝癌发生的风险呈正相关,已建立的肝癌血清标志物ELISA检测方法可用于肝癌高危人群的筛选及小肝癌的早期诊断,作为目前AFP和MRI诊断方法的有益补充。 | 王文 王锦红 缪晓辉 Mark A Feitelson 戚中田 | 2010 | 中国生物制品学杂志2010，23，3： | 4 |
| 7 | Hepatitis B virus integration, fragile sites, and hepatocarcinogenesis显示文摘 | Mark A. Feitelson Jungmin Lee | 2006 | Cancer Letters2006，，2： | 4 |
| 8 | 复方叶下珠对人HepG 2·2·15细胞移植裸鼠HBxAg表达的影响显示文摘 | 周大桥 童光东 贺劲松 魏春山 Feitelson Mark 吕屏 | 2006 | 中国中药杂志2006，31，19： | 4 |
| 9 | 精氨酸酶I在HCV转染肝癌细胞增殖中的作用显示文摘目的:研究丙型肝炎病毒(hepatitis C virus,HCV)基因组转染的肝癌细胞中精氨酸酶Ⅰ的表达及其意义,探究其在HCV-肝细胞肝癌(HCC)发病中的作用。方法:以转染HCV基因组的人肝癌细胞系(Huh7)为研究对象,采用蛋白印迹技术研究HCV基因组转染对细胞内精氨酸酶Ⅰ表达的影响;运用小干扰RNA(siRNA)技术抑制细胞精氨酸酶Ⅰ表达,并探讨其对细胞生长的影响及作用机制。结果:精氨酸酶Ⅰ在HCV阳性肝癌细胞系(Huh7-HCV)中的表达上调,且与对照细胞相比,Huh7-HCV细胞的精氨酸酶Ⅰ含量升高4.3倍。运用siRNA抑制细胞精氨酸酶Ⅰ表达,可明显抑制细胞生长并导致其死亡,且可使细胞周期发生明显改变。结论:精氨酸酶Ⅰ在HCV阳性肝细胞Huh7中表达上调,可能对促进Huh7-HCV细胞生长具重要意义。 | 曹文俊 Bill Sun 连兆瑞 Marcy Clayton Mark Feitelson 樊绮诗 | 2007 | 诊断学理论与实践2007，6，4： | 3 |
| 10 | 感染土拨鼠乙肝病毒的小鼠非瘤组织与肝细胞癌的差异表达基因显示文摘目的 确定土拨鼠HBV引发的肝癌组织和非癌组织中差异表达的基因。方法 通过抑制消减杂交法克隆土拨鼠HBV引发的肝癌组织和非癌组织中差异表达的基因 ;对差异表达基因进行DNA序列测定后于GeneBank内分析其同源性 ;应用原位杂交确定差异基因在肝癌组织和非癌组织中的特异性表达。结果 通过抑制消减杂交共得到了 14条肿瘤组织差异表达的基因片段。其中 ,肿瘤组织和非瘤组织共有的 8条基因与GeneBank中的已知基因同源 ,肿瘤组织来源的 5条基因和非瘤组织来源的 1条基因在GeneBank中未找到同源基因。原位杂交差异基因在肝癌组织和非癌组织中均为特异性表达。结论 通过抑制消减杂交获得了 14条肝癌组织和非癌组织差异表达的基因 。 | 曹晓燕 刘杰 连兆瑞 Marcy Clayton 胡加露 朱明华 樊代明 Mark Feitelson | 2001 | 陕西肿瘤医学2001，9，2： | 2 |
| 11 | Hepatitis B virus in hepatocarcinogenesis显示文摘 | Mark A FEITELSON | 1999 | Journal of cellular Physiology1999，18，： | 1 |
| 12 | 蛋白翻译起始因子C2在肝癌、胃癌中的表达与分布显示文摘目的 研究C2基因在肝细胞癌 (HCC)、胃癌中的表达、分布及意义。方法 利用免疫组化法检测C2蛋白在 6 0例HCC、5 8例胃癌组织中的表达 ,Westernblot法检测C2蛋白在 10例HCC及其癌旁组织中的表达。结果 6 0例HCC及 4 2例癌旁组织中 ,C2蛋白阳性率分别为 2 7.3% (17/ 6 0例 )和83.3% (35 / 4 2例 ) ,C2蛋白在HCC癌组织中表达明显低于其癌旁组织 (P <0 .0 0 1) ;C2的表达与病人年龄、HBsAg及AFP有明显关系 (P <0 .0 5 )。Westernblot结果与免疫组化一致。在HBXAg阳性的 4 9例HCC中 ,C2蛋白阳性率为 2 0 .4 % ,在HBXAg阴性的 11例HCC中 ,C2蛋白阳性率为6 3.6 %。C2在HBXAg阳性的HCC中的表达明显低于HBXAg阴性者 (P <0 .0 5 )。 5 8例原发性胃癌及 4 4例癌旁组织中 ,C2蛋白阳性率分别占 4 1.4 % (2 4 / 5 8例 )和 77.3% (34/ 4 4例 )。C2蛋白在胃癌组织中表达明显低于其癌旁组织 (P <0 .0 5 ) ,且与胃癌组织的分化程度、浆膜浸润、肿瘤大小有明显的关系 (P <0 .0 5 )。结论 C2基因表达下调可能与HCC、胃癌的发生、发展有关。HBXAg对C2的抑制作用可能与HCC的发生 ,发展有关。 | 张庆 刘杰 张力 李青 李勤 王新 乔泰东 樊代明 Mark Feitelson | 2002 | 中华消化杂志2002，22，5： | 1 |
| 13 | 合成多肽抗原检测原发性肝癌血清标志物ELISA方法的建立及应用显示文摘目的建立用合成多肽抗原检测原发性肝癌血清标志物的ELISA方法,并进行初步应用。方法利用筛选的5种与乙型肝炎病毒X抗原(HBx)诱导肝癌相关的细胞蛋白URG4、URG7、URG11、S15a和Sui1,作为原发性肝癌的筛查和早期诊断的血清标志物,根据上述蛋白的序列合成多肽(L4A/L4B、L7B、L11-1/L11-3/L11-4、L12A/L12B和Sui1A/Sui1B),作为检测抗原,建立检测相应抗体的间接ELISA法,并进行敏感性、特异性、精密性评价及临床应用。结果所建立的间接ELISA法敏感性为93.8%,特异性为97.9%,试验内和试验间变异系数分别为3.8%~5.6%和7.4%~10.3%;检测161份肝癌、肝硬化及乙型肝炎患者血清样本中,1种指标以上阳性检出率分别为90.4%、92.6%和61.7%,2种指标以上阳性检出率分别为78.6%、70.6%和48.3%;39份正常献血员血清中,1种指标以上阳性检出率为12.2%,2种指标以上阳性检出率为6.3%。结论所建立的ELISA法可作为目前的AFP和核磁共振诊断方法的有益补充,用于原发性肝癌高危人群的筛选和小肝癌的早期诊断。 | 王文 王锦红 缪晓辉 Mark A Feitelson 戚中田 | 2009 | 中国生物制品学杂志2009，22，4： | 1 |
| 14 | Putative roles of hepatitis B x antigen in the pathogenesis of chronic liver disease显示文摘 | Mark A. Feitelson Helena M.G.P.V. Reis N. Lale Tufan Bill Sun Jingbo Pan Zhaorui Lian | 2008 | Cancer Letters2008，，1： | 1 |
| 15 | HCV感染相关的肝细胞性肝癌中精氨酸酶Ⅱ的表达显示文摘目的通过对丙型肝炎病毒-原发性肝细胞肝癌(HCV-HCC)组织及细胞中精氨酸酶Ⅱ(Arg-Ⅱ)的表达进行分析,并以RNA干扰技术阻断其在细胞内的表达,初步研究Arg-Ⅱ表达在HCV-HCC发病中的意义。方法首先以基因转染技术分别将HCV基因组和对照质粒导入HuH7细胞中,以逆转录-实时荧光PCR检测HCV基因组的转录并作细胞生长曲线测定,以Western blotting技术研究HCV基因组转染对细胞内Arg-Ⅱ表达的影响,以免疫组化技术分析HCV-HCC组织中Arg-Ⅱ的表达水平,运用RNA干扰技术对Arg-Ⅱ作初步的功能分析。结果以基因转染技术分别将HCV基因组和对照质粒导入HuH7,成功建立了HuH7-HCV和HuH7-vector两个细胞系,逆转录-实时荧光PCR检测表明HuH7-HCV细胞的HCV转录水平为0.5~5拷贝/细胞。Western blotting结果显示,与对照细胞相比,HuH-7-HCV细胞的Arg-Ⅱ含量升高3.9倍。免疫组化技术分析HCV-HCC组织标本中Arg-Ⅱ的表达,结果呈强阳性,而对照标本中基本不表达。采用RNA干扰方法阻断HuH7-HCV细胞的Arg-Ⅱ表达,发现细胞增殖被明显抑制。结论Arg-Ⅱ在HCV阳性肝细胞系中及HCV-HCC组织中异常表达并可能参与HCV-HCC的发病机制。 | 曹文俊 Bill Sun 徐锋 连兆瑞 Marcy Clayton Mark Feitelson 樊绮诗 | 2007 | 上海交通大学学报(医学版)2007，27，8： | 1 |
| 16 | Hepatitis B virus in hepatocarcinogenesis显示文摘 | Mark A Feitelson | 1999 | Cellular Physiology1999，181，： | 1 |
| 17 | The roles of hepatitis B virus-encoded X protein in virus replication and the pathogenesis of chronic liver disease显示文摘 | Mark A Feitelson Barbara Bonamassa Alla Arzumanyan | 2014 | Expert Opinion on Therapeutic Targets2014，，3： | 1 |
| 18 | Hepatitis B virus in hepatocarcinogenesis显示文摘 | Mark A Feitelson | 1999 | CeUular Physiology1999，181，： | 1 |
| 19 | Hepatitis B virus integration, fragile sites, and hepatocarcinogenesis显示文摘 | Mark A. Feitelson Jungmin Lee | 2006 | Cancer Letters2006，，2： | 1 |
| 20 | Preclinical Characterization of GLS4, an Inhibitor of Hepatitis B Virus Core Particle Assembly显示文摘 | Guoyi Wu Bo Liu Yingjun Zhang Jing Li Alla Arzumanyan Marcia M. Clayton Raymond F. Schinazi Zhaohe Wang Siegfried Goldmann Qingyun Ren Faxhou Zhang Mark A. Feitelson | 2013 | Antimicrobial Agents and Chemotherapy2013，，11： | 1 |
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