ObjectiveTo study the epidemiologic characteristics of primary liver cancer (PLC). MethodsThe literatures about regional distribution and etiologic epidemiology of PLC were reviewed. Results PLC was mainly distributed on caostland in the south-east of China. The main cause of PLC was hepatitis B virus, aflatoxin and contamination of drinking water. Otherwise, PLS was also related with lack of some trace element, sex horemones, genealogy cause and so on.Conclusion The genesis of PLC was by multiple factors.
【Abstract】Objective To investigate the apoptosis induced by TGF-β1 in human hepatic carcinoma cell lines and its relationship with p53 gene and Smad. Methods Three human hepatic carcinoma cell lines which involving in various status of the p53 gene were used in this study. TGF-β1-induced apoptosis in hepatic carcinoma cell lines was measured by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. To study the mechanism of TGF-β1-induced apoptosis, these cell lines were transfected with a TGF-β1-inducible luciferase reporter plasmid containing Smad 4 binding elements (SBE) and luciferase gene using Lipofectamine 2000, then treated with TGF-β1, relative luciferase activity was assayed. Results Of three cell lines studied with TUNEL assay, TGF-β1 induced apoptosis was observed in HepG2 cells (wild type p53). Huh-7 (mutant p53) and Hep3B (deleted p53) cell lines showed less apoptosis. Luciferase activity assay indicated that the response to TGF-β1 induction in HepG2 cells was increased dramatically but was not significant in Huh-7 and Hep3B cell lines. Conclusion HepG2 cells seem to be highly susceptible to TGF-β1-induced apoptosis compared with Hep3B and Huh7 cell lines. Smad 4 is a central mediator of the TGF-β1 signal transduction pathway.
ObjectiveTo investigate the predicting effect of PIK3CA mutations for the efficacy and prognosis of hepatocellular carcinoma (HCC) patients received surgical resection. MethodsPCR and DNA sequencing were used to detect the PIK3CA mutation status of 79 HCC tissues, its impact on the short and long term effects of the patients were analyzed. ResultsIn this group of patients, mutation rate of PIK3CA gene exon 9 was 39.24% (31/79), PIK3CA mutation rate correlated with lymph node status and tumor differentiation (P < 0.05). The therapeutic effect of patients with PIK3CA mutation was significantly poor than that of the non-mutated group (P < 0.05). The three-year cumulative survival of patients with PIK3CA mutation (33.33%) was significantly lower than non-mutated group's (60.00%) by Kaplan-Meier (P < 0.05). ConclusionPIK3CA gene mutation in exon 9 could impact the efficiency of surgical resection in patients with HCC and could predict a poor survival prognosis.
Objective To clarify relationship between signal heterogeneity on hepatobiliary phase of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced MRI and prognosis of hepatocellular carcinoma (HCC). Methods From January 2014 to January 2017 in the First Affiliated Hospital of Chongqing Medical University, a total of 77 patients with the pathologically proved HCC underwent Gd-EOB-DTPA-enhanced MRI prior to surgery were included in this study. On the basis of the signal heterogeneity in the hepatobiliary phase, the included patients were designed to homogeneous hypointensity group and heterogeneous hyperintensity group. The disease-free survival time were compared between the 2 groups and it’s influencing factors were analyzed. Results Seventy-seven patients with HCC were included, including 45 cases of homogeneous hypointensity and 32 cases of heterogeneous hyperintensity. There were no significant differences in the age, gender, etiology, liver function, alpha-fetoprotein, differentiated degree, Child-Pugh grade, lesion diameter, lesion border, and number of lesions between the 2 groups (P>0.05). However, the HCC patients with heterogeneous hyperintensity had a later BCLC staging (P=0.001). The disease-free survival time of the patients with homogeneous hypointensity and heterogeneous hyperintensity was (17.0±9.8) months and (12.4±10.4)months, respectively. The Kaplan-Meier survival curve showed that the disease-free survival time in the patients with homogeneous hypointensity was significantly better than that in the patients with heterogeneous hyperintensity (P=0.020). The results of univariate analysis showed that the other confounding factors had no effect on the disease-free survival time of patients with hepatocellular carcinoma (P>0.05) except for the signal of hepatobiliary phase (P<0.05). Furthermore, the hepatobiliary phase signal, BCLC stage, and degree of differentiation, which might be clinically considered as potentially influencing for the prognosis of patients with HCC, were included in the Cox multivariate proportional hazard regression model and found that the heterogeneous hyperintensity was still the risk factor of the disease-free survival rate in patients with HCC (P=0.047). Conclusion Signal heterogeneity on hepatobiliary phase of Gd-EOB-DTPA-enhanced MRI is related to prognosis of patients with HCC, heterogeneous hyperintensity may indicate a lower disease-free survival rate.
目的探讨肝癌手术切除后的序贯综合治疗,以达到有效防治肿瘤复发的目的。方法从我科收治的肝癌患者中挑选3例手术治疗后进行序贯综合治疗并取得良好效果病例，对其临床资料进行分析，从中获取有关肝癌术后治疗的经验。结果3例肝癌患者在我科手术后接受了积极的预防复发措施，虽最终均出现复发，但对待复发的肿瘤均采取积极的应对措施，获得了长期生存。结论对于肝癌手术切除后的患者进行积极的序贯性综合治疗有较好的临床意义，鼓励对术后复发病例进行积极序贯综合治疗。
【Abstract】ObjectiveTo study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC). MethodsArticles have been reviewed to find out the theory of spontaneous rupture of HCC. ResultsResearchful results suggested that the injury of small arteries was usually followed in patients of spontaneous rupture of HCC. In this review, the immune complex, which composed of hepatitis B virus e antigen, complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of immune complex deposition, vascular injury occurs mainly in the small arteries where the deposition of immune complex was present. The small arteries in which immune complex deposited are readily injuried and cause hemorrhage and rupture of HCC during vascular load increase. ConclusionWe would conclude that immune complex deposition in vessel wall led to the small arteries injury may be the factor involved in the pathogenesis of spontaneous ruptured HCC.