中文摘要：

主要的肝癌症为世界范围的全部的肝癌症的 70%-85% 是癌症死亡，和 hepatocellular 癌(HCC ) 报道的一个重要原因。长期的肝炎 B 病毒(HBV ) 感染贡献 >75% HCC 盒子。高浆液病毒的负担是在预言 HCC 的开发的病毒的复制的最可靠的指示物。HBV 遗传型 C 仔细在肝脏硬化症的病人与 HCC 被联系 > 50 年，而遗传型 B 在非肝脏硬化症的年轻病人和 HCC 的手术后的恶化与 HCC 的开发被联系。不同 HBV subgenotypes 变化的不同模式，它清楚地与被联系增加了 HCC 的风险。变化在长期的 HBV 感染期间积累并且预言 HCC 的出现。长期的发炎经由细胞的 cytidine 脱氨基酶正式就职导致病毒的变化的增加的频率。变化被主人免疫否定地选择，而一些逃跑免疫的 HBV 异种在 hepatocarcinogenesis 是活跃的。煽动性的小径贡献 inflammation-necrosis-regeneration 过程，最终 HCC。他们的特点分子能在感染 HBV 的题目预言恶意。持续发炎与复发和转移有关涉及 hepatocarcinogenesis 并且仔细。在 HBV 相关的 HCC 纸巾的煽动性的分子的 HBV 负担，遗传型 C，病毒的变化和表示显著地与差的预后被联系。在在 peritumoral 纸巾的 intratumoral CD8+ T 房间和规章的 T 房间或 Th1 和 Th2 cytokines 之间的不平衡能预言 HBV 相关的 HCC 的预后。这些因素为开发更可能开发 HCC 的感染 HBV 的题目的活跃预防和监视，或为定制合适的处理改进幸存或推迟 HCC 的手术后的复发是重要的。

英文摘要：

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 Thl 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.