Objective To systematically evaluate the effectiveness and safety of laparoscopic hepatectomy (LH) versus open hepatectomy (OH) for hepatocellular carcinoma (HCC). Methods Databases including PubMed, EMbase, MEDLINE, SCI, CNKI, CBM, WanFang Data and The Cochrane Library (Issue 3, 2012) were searched to collect the randomized controlled trails (RCTs) and non-RCTs about LH versus OH for HCC. The retrieval time was from inception to August 2012. The studies were screened according to the inclusion and exclusion criteria, the data were extracted and the quality was evaluated by 2 reviewers independently. Then the meta-analysis was conducted using RevMan 5.1 software. Results A total of 13 non-RCTs involving 701 patients were included. The results of meta-analysis showed that: Compared with OH, LH had lesser amount of intraoperative bleeding (MD=?144.09, 95%CI ?194.25 to ?93.94, Plt;0.000 01), shorter hospital stay (MD=?5.48, 95%CI ?7.10 to ?3.85, Plt;0.000 01), and lower postoperative complications (OR=0.43, 95%CI 0.27 to 0.66, P=0.000 1). But there were no differences between the 2 groups in operation time (MD=?0.64, 95%CI ?22.95 to 21.68, P=0.96), perioperative death rate, 3-5 year survival rate, and tumor free survival rate. Conclusion LH is superior to OH in treating HCC for it is associated with smaller wound, lesser operative blood loss, shorter hospital stay, and lower postoperative complications. And it is similar as OH in operation time, perioperative death rate and 3-5 year survival rate. So LH is safe and feasible for treating HCC when its indications are strictly controlled. However, for the quantity and quality limitation of the included studies, this conclusion still requires to be further proved by performing large scale and high quality RCTs. It suggests that doctors should choose a best therapy for HCC patients according to an integrative disease assessment.
Objective To evaluate the efficiency and safety of laparoscopic hepatectomy (LH) and conventional open hepatectomy (OH) in patients with hepatocellular carcinoma (HCC). Methods We searched The Cochrane Library, MEDLINE (1966~2008.3), EMBASE (1966~2008.3), CBM (1979~2008.3), we also handsearched some Chinese journals. Using a defined search strategy, randomized controlled trails and controlled clinical trials of comparing OH with LH for hepatocellular carcinoma were identified. Data were extracted and evaluated by two reviewers independently. The quality of the included trails was evaluated by Deeks JJ’s evaluation criterion. Meta–analysis was done using the Cochrane collaboration’s Revman 4.2.10. Results Seven controlled clinical trials (309 patients) were included, The meta–analysis showed that: (1) Four studies (n=198) reported mortality, the mortality rate of the LH group was not significantly different from that of the OH group [OR=1.14, 95%Cl (0.15, 8.65), P=0.90]; (2) Two studies (n=91) reported blood transfusion. There were no significant differences between the two treatment groups in terms of the blood transfusion [OR=0.20, 95%Cl (0.03, 1.19), P=0.08]; (3) Four studies (n=165) reported operation time. There were significant differences in operating time between the two groups [SMD=1.05, 95%CI (0.72, 1.38), Plt;0.000 01]; (4) Four studies (n=165) reported intraoperative blood loss. There were significant differences in intraoperative blood loss between the two groups [SMD= – 1.56, 95%Cl (– 2.39, – 0.73), P=0.000 2]; (5) Five studies (n=210) reported the duration of hospital stay. There were significant differences in duration of hospital stay between the two groups [WMD= – 3.89, 95%CI (– 5.54, – 2.23), Plt;0.000 01]; (6) Two studies (n=248) reported complications. There were significant differences in complications between the two groups [OR=0.31, 95%Cl (0.13, 0.72), P=0.006]; (7) Two studies (n=97) reported ALT. There were significant differences in ALT between the two groups [SMD= – 1.54, 95%Cl (– 207, – 1.01), Plt;0.000 01]. Conclusion LH is associated with less postoperative complications, operative blood loss, duration of hospital stay and lower ALT, but longer operation time. However, the trails available for this systematic review are limited, so a prospective randomized controlled trial is warranted to fully investigate these and other outcome measures.
Objective To explore the relationship between the HBsAg positive patients suffering from hepatocellular carcinoma (HCC) and HBV DNA genotype. Methods By using PCR type-specific primers combined with sequencing of genotype, we analyzed the genotype of HBV DNA in the serum of 500 patients with positive HBsAg in our hospital. Among them, 150 cases suffered from HCC. Results Genotype B and C were both predominant genotypes in HBsAg positive patients. But in HCC group, the rate of genotype C was 65.33% （98/150）, which was significantly higher than that in non-HCC group (88/350, 25.14%), while genotype B, in contrast, was 28.67% （43/150） and 68.86% （241/350）， χ2=75.45， Plt;0.05. The distribution of HBV DNA genotype B or genotype C in different gender or different age groups were not statistically significantly different in cases of HCC (Pgt;0.05). Conclusion Genotype C of HBV DNA is more common in patients with HCC, and maybe there is relationship between genotype C and the occurrence of HCC.
ObjectiveTo investigate the expressions and clinical significance of human telomerase reverse transcriptase (hTERT) mRNA and γglutamyl transpeptidase mRNA-H (GGT mRNA-H) in the peripheral blood of small hepatocellular carcinoma (HCC) patients. MethodsThe expressions of hTERT mRNA and GGT mRNA-H were detected in the peripheral blood of thirty patients with small HCC by RT-PCR, eighteen patients with benign liver diseases, and twelve normal volunteers. ResultsThe positive rate of hTERT mRNA and GGT mRNA-H expression in patients with small HCC were 80.0% (24/30) and 46.7%(14/30), respectively. In patients with hepatitic cirrhosis the positive rate of hTERT mRNA expression was 33.3% (6/18), while the expression of GGT mRNA was not detected. Both the expressions of hTERT mRNA and GGT mRNA-H were negative in all normal volunteers. The combination analysis of hTERT mRNA and GGT mRNA-H expression achieved positive rate of 86.7% in the diagnosis of small HCC, which was significantly higher than the positive rate of AFP (26.7%)， Plt;0.05. ConclusionThe hTERT mRNA and GGT mRNA-H are significantly expressed in small HCC patients, the combination analysis of hTERT mRNA and GGT mRNA-H seems to be useful in the early diagnosis of small HCC.
ObjectiveTo determine the risk factors for recurrence of hepatocellular carcinoma (HCC) after orthotopic liver transplantation (OLT). MethodsThe clinical data from seventysix consecutive HCC patients who underwent OLT were retrospectively analyzed. The patients were divided into nonrecurrence group (n=53) and recurrence group (n=23) based on recurrence, and the characteristics of tumor recurrence were analyzed. ResultsThe overall recurrence rate of tumor was 30.3% (23/76). By univariate analysis, gender (P=0.449), age (P=0.091), received preoperative therapy or not (P=0.958), tumor numbers (P=0.212), and HBV/HCV infection (P=0.220) were not closely related with tumor recurrence, while the integrality of tumor capsule (P=0.009), tumor stage (P=0.002), tumor diameter (Plt;0.001), vascular invasion (Plt;0.001), and AFP level before transplantation (P=0.044) were significantly related with tumor recurrence. Furthermore, the oneyear recurrence rate of tumor was higher in patients whose AFP level returned to normal within two months after transplantation (Plt;0.001) and tumor diameter was less than 5.0 cm (P=0.001). Multivariate analysis revealed that tumor diameter (P=0.001, OR=6.456, 95%CI: 2.356-17.680), vascular invasion (P=0.030, OR=10.653, 95%CI: 1.248-90.910), and AFP level before transplantation (P=0.017, OR=2.601, 95%CI: 2.196-5.658) were independent risk factors for tumor recurrence. ConclusionMore attentions shall be paid to these patients with tumor diameter gt;5.0 cm, vascular invasion, and AFP level before transplantation ≥400 μg/L, in particular AFP level is beyond normal within two months after transplantation, and antitumor therapy shall be given as soon as possible.
ObjectiveTo study the mechanisms of spontaneous rupture of hepatocellular carcinoma and the treatments in the acute phase and the second phase after hemostasis. MethodsRelated domestic and foreign literatures were reviewed. ResultsThe mechanism of spontaneous rupture of hepatocellular carcinoma was still not quite clear. In China, spontaneous rupture of hepatocellular carcinoma was closely related with hepatitis B virus infection. Immune complex deposition in vessel wall led to the injuries of small arteries and bleeding. Treatments included conservative therapy, surgical intervention （lobectomy of liver, hepatic artery ligation, packing, and suturing), transarteial embolization, other medications (percutaneous ethanol injection, radiofrequency ablation, bio-immunotherapy). ConclusionTransarterial embolization has been shown to be highly effective in achieving immediate hemostasis, and can be used as the basis of phase two comprehensive treatment.
Objective To construct a mammalian vector encoding angiostatin kringle 5 (K5) under the control of αfetoprotein （AFP） enhancer and albumin promoter, and to observe the expression of angiostatin by introducting angiostatin gene into hepatocellular carcinoma cells through gene transfection. Methods Angiostatin cDNA was amplified from normal human eukaryotic cells by using RTPCR. Meanwhile, AFP enhancer and albumin promoter sequences were directed cloned and were inserted into vector pcDNA3.1. The recombinant vector of pcDNA3.1AFABangiostatin K5His was constructed, which contained the angiostatin K5 cDNA sequence that was under the control of the AFP enhancer and promoter. Angiostatin K5 cDNA was introduced into human AFP positive hepatocellular carcinoma cell lines with the transfected cultured cells that were mediated with Lipofectamine 2000. The expression of angiostatin K5 was analyzed by Western blot and the protein was dectected with antiHis antibody. Results The 500base pair of angiostatin K5 was in accordance with the expected sequence and the recombinant vector of pcDNA3.1AFABangiostatin K5His was also confirmed as the anticipated sequence. The expression of angiostatin K5 in AFP positive hepatocellular carcinoma cells was detected both by SDSPAGE and Western blot. Conclusion Efficient construction and expression of angiostatin K5 to AFP positive cells make it possible for antiangiogenesis therapy of human hepatocellular carcinomas, which may provide a promising approach.
Objective To study the expression of proliferating cell nuclear antigen (PCNA) in the occurrence and development of hepatocellular carcinoma. Methods Sixty SD rats were randomly divided into control group and experimental group. 3′MeDAB was administrated into rats to establish the experimental model of hepatocarcinoma. The expressions of PCNA of different phases were detected by immunohistochemistry and the liver pathologic changes were observed by optical microscope. Results The process of canceration was divided into three stages: inflammation, proliferative fibrosis and hepatic carcinoma. The expression of PCNA firstly presented in the oval cells that located in the portal area at the stage of inflammation, and a part of PCNA were hyperexpressed in the portal area. The expression rate of PCNA in the middle phase of inflammatory stage was higher than that of any other phases but declined later. Yet, when it came to the stage of hepatic carcinoma, the rate increased again. Conclusion Under the experimental circumstance when liver cancer is caused by the carcinogenic agent, PCNA may be firstly expressed in the oval cells, and the dynamic expression of PCNA may be an indicator for the early diagnosis of hepatocarcinogenesis.
Objective To identify genes associated with hepatocellular carcinoma (HCC) as candidate diagnostic markers in a genome-wide scale. Methods The gene expression profiles of 40 pairs of HCC tumor tissue and peripheral non-tumorous liver tissue were analyzed by using gene chip technology.The gene chips were fabricated at the National Cancer Institute (NCI). Each gene chip contained 9 180 genes. The fluorescent targets were prepared by a direct labeling approach using two kinds of fluorescences as following: 100 μg of total RNA from non-cancerous liver tissue was labeled with Cy3-dUTP and 200 μg of total RNA from HCC was labeled with Cy5-dUTP. The targets were mixed together and hybridized with genes on the gene chips. Unsupervised hierarchical clustering analysis was done by CLUSTER and TREEVIEW software using median centered correlation and complete linkage. Results A total of 10 genes were found up-regulated in over 80% of primary tumors comparing with that of their corresponding non-tumorous liver tissues at a two-fold filter with an unsupervised hierarchical clustering algorithm, including protocadherin-alpha 9, ESTs, Homo sapiens cDNA FLJ, KPNA2, RPS20, SNRPE, CDKN2A, UBD, MDK and ANXA2.Conclusion These genes are supposed to be candidates for the diagnosis of HCC. Further investigation of these genes in a large scale of patients with HCC and patients with non-malignant hepatic diseases will be needed to disclose whether they could be used clinically as novel diagnostic tumor markers for HCC.
Objective To establish hepatocellular carcinoma (HCC) cell lines which olig-expressed IGF1R gene stably． Methods An eukaryotic expressing vector pSUPER-IGF1R-siRNA that could block IGF1R expressing was transferred into hepatocellular carcinoma cell lines SMMC7721 and Hep3B with Lipofectamine 2000 reagents． After transferred, cells were selected with G418 to obtain positive clones. The expressions of IGF1R, cyclin D1 and cyclin B1 were detected by RT-PCR and Western-blot． Cell growth curve were painted. Results Two cell lines clones were screened olig-expressing IGF1R gene stably． The experimental cell lines grew more slowly than control cell lines and the expression of cyclin D1 decreased (P＜0.05). Conclusion The HCC cell lines for olig-expressing IGF1R gene stably are established successfully．The plasmid pSUPER-IGF1R-siRNA can inhibit the growth of SMMC7721 and Hep3B cell lines, and the expression of cyclin D1.