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| 1 | Role of hepatitis B virus DNA integration in human hepatocarcinogenesis显示文摘Liver cancer ranks sixth in cancer incidence,and is the third leading cause of cancer-related deaths worldwide.Hepatocellular carcinoma(HCC)is the most common type of liver cancer,which arises from hepatocytes and accounts for approximately 70%-85%of cases.Hepatitis B virus(HBV)frequently causes liver inflammation,hepatic damage and subsequent cirrhosis.Integrated viral DNA is found in 85%-90%of HBV-related HCCs.Its presence in tumors from non-cirrhotic livers of children or young adults further supports the role of viral DNA integration in hepatocarcinogenesis.Integration of subgenomic HBV DNA fragments into different locations within the host DNA is a significant feature of chronic HBV infection.Integration has two potential consequences:(1)the host genome becomes altered('cis'effect);and(2)the HBV genome becomes altered('trans'effect).The cis effect includes insertional mutagenesis,which can potentially disrupt host gene function or alter host gene regulation.Tumor progression is frequently associated with rearrangement and partial gain or loss of both viral and host sequences.However,the role of integrated HBV DNA in hepatocarcinogenesis remains controversial.Modern technology has provided a new paradigm to further our understanding ofdisease mechanisms.This review summarizes the role of HBV DNA integration in human carcinogenesis. | Hoang Hai Akihiro Tamori Norifumi Kawada | 2014 | World Journal of Gastroenterology2014，20，20： | 22 |
| 2 | Natural regression of fibrosis in chronic hepatitis B显示文摘The fibrosis of liver cirrhosis was considered to be irreversible before the anti-viral drugs showed that it is reversible when they lead to continuous suppression of viral replication and inflammation. However, several reports previously showed that fibrosis of type B liver cirrhosis was almost completely absorbed after the natural remission of chronic inflammation. This phenomenon might not be limited to exceptional patients, but rather occur commonly, considering the dynamic clinical features of chronic hepatitis B(CHB), where inactive carrier stage normally follows aggravation of hepatitis and progression of fibrosis at the time of HBe Ag seroconversion. Thus, fibrosis levels of CHB as a hepatocellular carcinoma(HCC)-surveillance marker, particularly those of the inactive stage, could be underestimated, because some of them might have been(pre)cirrhotic in the past and recovered with the natural regression of fibrosis. We argue that cirrhosisinduced HCC mechanisms, rather than direct action of viral genome, may be more common than generally considered in CHB patients. This may have some impact on reconsidering the surveillance rationale for HCC in CHB, from where advanced HCCs tended to be missed. In addition, a molecular marker to assess the cancer-prone characteristics of the liver will definitely be needed to resolve the issue. | Shogo Ohkoshi Haruka Hirono Kazuhiko Watanabe Katsuhiko Hasegawa Kenya Kamimura Masahiko Yano | 2016 | World Journal of Gastroenterology2016，22，24： | 8 |
| 3 | 乙型肝炎表面抗原阳性对免疫抑制状态下小鼠肝癌复发的影响显示文摘目的比较免疫抑制状态下血清学乙型肝炎表面抗原(HBs Ag)阳性与阴性小鼠肝脏肿瘤的复发及进展情况,为临床应用HBs Ag阳性供肝行肝移植治疗以挽救晚期肝癌患者的可行性提供理论依据。方法实验组选用乙型肝炎病毒(HBV)转基因Balb/c小鼠30只,对照组选用普通Balb/c小鼠30只,每组分别给予脾包膜下接种H22肿瘤细胞株,术后给予环孢素A、甲泼尼龙琥珀酸钠进行免疫抑制干预治疗,模拟肝移植术后免疫抑制状态,至观察结束。分别于术后1、2、3周处死小鼠,观察比较两组小鼠肿瘤复发率、荷瘤肝重;苏木素-伊红(HE)染色观察肿瘤组织形态;免疫组化检测肝组织增殖细胞核抗原(PCNA)、血管内皮生长因子(VEGF)及细胞间黏附分子-1(ICAM-1)的表达。结果两组小鼠肿瘤复发率:实验组术后1、2、3周分别为20%、50%、80%,对照组术后1、2、3周分别为20%、40%、70%;荷瘤肝重:实验组术后1、2、3周分别为(1.04±0.05)g、(1.16±0.06)g、(1.29±0.06)g,对照组术后1、2、3周分别为(1.01±0.06)g、(1.13±0.05)g、(1.25±0.08)g;肝组织PCNA阳性指数:实验组术后1、2、3周分别为22.20%±5.85%、44.20%±6.07%、53.40%±7.92%,对照组术后1、2、3周分别为22.80%±5.51%、43.60%±6.95%、56.80%±9.14%;VEGF阳性指数:实验组术后1、2、3周分别为20.80%±5.47%、25.90%±5.51%、37.60%±2.16%,对照组术后1、2、3周分别为17.00%±4.14%、26.70%±6.40%、37.30%±1.42%;ICAM-1阳性指数:实验组术后1、2、3周分别为15.40%±3.89%、23.20%±3.61%、31.30%±3.47%,对照组术后1、2、3周分别为14.50%±3.41%、22.80%±2.97%、29.40%±3.69%;实验组和对照组比较差异均无统计学意义(均P>0.05)。结论通过对免疫抑制状态下HBV转基因Balb/c小鼠移植型肿瘤复发动物模型的观察研究,认为血清学HBs Ag阳性对小鼠肝癌复发及生长无显著影响。 | 高伟 葛亮 | 2015 | 实用器官移植电子杂志2015，3，1： | 3 |
| 4 | New horizon for radical cure of chronic hepatitis B virus infection显示文摘About 250 to 350 million people worldwide are chronically infected with hepatitis B virus(HBV), and about 700000 patients per year die of HBV-related cirrhosis or hepatocellular carcinoma(HCC). Several anti-viral agents, such as interferon and nucleos(t)ide analogues(NAs), have been used to treat this disease. NAs especially have been shown to strongly suppress HBV replication, slowing the progression to cirrhosis and the development of HCC. However, reactivation of HBV replication often occurs after cessation of treatment, because NAs alone cannot completely remove covalentlyclosed circular DNA(ccc DNA), the template of HBV replication, from the nuclei of hepatocytes. Anti-HBV immune responses, in conjunction with interferon-γ and tumor necrosis factor-α, were found to eliminate ccc DNA, but complete eradication of ccc DNA by immune response alone is difficult, as shown in patients who recover from acute HBV infection but often show long-term persistence of small amounts of HBV-DNA in the blood. Several new drugs interfering with the life cycle of HBV in hepatocytes have been developed, with drugs targeting ccc DNA theoretically the most effective for radical cure of chronic HBV infection. However, the safety of these drugs should be extensively examined before application to patients, and combinations of several approaches may be necessary for radical cure of chronic HBV infection. | Kazuto Tajiri Yukihiro Shimizu | 2016 | World Journal of Hepatology2016，8，21： | 1 |
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