Analysis of the molecular mechanism of hepatocarcinogenesis in patients with chronic viral diseases and its application for genetic diagnosis of hepatocellular carcinoma.

包括I类B54在内的扩展单倍型被证明与肝损伤的进展相关，而包括II类DRB 1 ^*1302-DQB 1 ^*0604和TAP 2 ^*0103在内的扩展单倍型与慢性HCV感染中的低肝炎活性相关。因此，单核苷酸多态性可能与慢性HCV感染患者肝脏疾病的发生和/或进展有关。MAPK/ERK在人肝细胞癌（HCC）中的激活被证明在多步骤肝癌发生中起重要作用，尤其是在HCC的进展中，细胞周期蛋白D1的上调主要由MAPK/ERK通过c-来自HCV感染患者的树突状细胞的刺激潜能针对同种异体抗原而不是针对回忆抗原受损。这种损害的可能机制是它们在基线时的CD 86和/或IL-12的低表达，并且低同种异体应答可以通过添加IL-2或IL-12来克服。然而，当dendr ...更多信息 来自HCV感染患者的IC细胞遇到回忆抗原，它们被激活以恢复细胞因子产生和刺激T细胞增殖的潜力。B7-1转染的肝癌细胞与IL-12联合免疫可诱导针对亲代肝癌细胞的保护性和治疗性免疫，这一联合治疗可能有助于抑制肝癌复发。干扰素治疗可降低慢性丙型肝炎患者的肝癌发病率，表现为ALT一过性恢复正常，干扰素治疗结束后ALT持续恢复正常。此外，生存分析和死亡原因的确定表明，干扰素治疗提高了长期生存的慢性丙型肝炎患者谁响应这种治疗，可能通过降低死亡率从肝脏相关疾病，这些研究结果可能会导致澄清肝损害和肝细胞癌的发展机制，并改善慢性丙型肝炎感染患者的长期临床结果。少

Extended haplotypes including class I B54 is demonstrated to be associated with the progression of liver injury, whereas extended haplotypes including class II DRB1^*1302-DQB1^*0604 and TAP2^*0103 to be associated with low hepatitis activity in chronic HCV infection. Thus, single nucleotide polymorphism may be related to the development and/or progression of liver disease in patients with chronic HCV infection.MAPK/ERK activation in human hepatcellular carcinoma (HCC) is shown to play an important role in multistep hepatocarcinogenesis, especially in the progression of HCC through cyclin D1 up-regulation primarily induced by MAPK/ERK via c-fos.The stimulatory potentials of dendric cells from patients with HCV infection are impaired against alloantigens but not against recall antigens. The possible mechanism for such impairment are their low expression of CD86 and/or IL-12 at the baseline, and low allogenic response could be overcome by the addition of IL-2 or IL-12. However, when dendr … More ic cells from patients with HCV-infection encounter recall antigens, they are activated to restore the potentials for cytokine production and stimulation of T cell proliferation. The combination of immunization of B7-1-transfected HCC cells and IL-12 could induce protective and therapeutic immunity against parental HCC cells, and this combination therapy may be useful for suppressing recurrence of HCC.Interferon therapy lowered the incidence of HCC among ratients with chronic hepatitis C showing transient normalization of ALT as well as sustained normalization of ALT after the completion of interferon therapy. Moreover, survival analyses and determination of cause of death suggest that interferon therapy improves the long-term survival of chronic hepatitis C patients who responded to this therapy, possibly by decreasing mortality from liver-related diseases.These findings may lead to clarify the mechanism of the development of liver damage and hepatocellular carcinoma and to improve the long-term clinical outcome of patients with chronic HCV infection. Less