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<p><b>BACKGROUND</b>The aim of this research was to analyze the perioperative factors of regular hepatectomy and irregular hepatectomy. The superiority of the clinical application of the two methods was compared in the perioperative period.</p><p><b>METHODS</b>From 1986 to 2011, 1798 patients underwent consecutive liver resections with regular hepatectomy and irregular hepatectomy at the Air Force General Hospital of People's Liberation Army and the General Hospital of Chinese People's Liberation Army. Their medical documentation was investigated retrospectively.</p><p><b>RESULTS</b>In patients on whom regular hepatectomy and irregular hepatectomy were performed, there was no significant difference in perioperative blood loss, complications, in-hospital mortality, hospital stay, and so on. But in regular hepatectomy, operating time was an independent risk factor (P < 0.001, OR = 1.004).</p><p><b>CONCLUSIONS</b>There was no significant difference between the perioperative risk of regular hepatectomy and that of irregular hepatectomy.</p>
Subject(s)
Female , Humans , Male , Hepatectomy , Methods , Perioperative Period , Retrospective StudiesABSTRACT
The mechanism and interaction among Rb/p16, Rb/E2F1 and HDAC1 proteins in gallbladder carcinoma were investigated. By using the immunoprecipitation method, the interactions among Rb, p16, E2F1, HDAC1 proteins in gallbladder carcinoma cell line (Mz-ChA-1) were studied. It was found that there were Rb and E2F1 proteins in the precipitates with anti-HDAC1, and there were HDAC1 and E2F1 proteins in the precipitate with anti-Rb. It was concluded that there are specific interactions among Rb, HDAC1 and E2F1 proteins in gallbladder carcinoma, indicating the existence of the direct Rb/E2F1/HDAC1 signal transduction pathway. There is no direct relationship between p16 proteins with Rb, HDAC1, and E2F1 proteins.
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Objective To summarize experiences associated with hepatectomy of huge liver neoplasm.Methods Two hundred and sixty six consecutive cases of huge liver neoplasm undergoing hepatectomy from January 1987 to December 2005 at Chinese PLA General Hospital were analized retrospectively based on the clinical data.Results There were 174 males and 92 females with the average age of(44.8 ± 12.2)years(range 7-76 yrs).Among them,93 cases were with benign neoplasms.The maximum diameter of tumors was 30 cm and hemangioma accounted for 86.0%(80 cases).The other 173 cases were huge liver malignant neoplasms with the maximum diameter of 33 cm,hepatocellular carcinoma accounted for 73.4%(127 cases).The average diameter of all tumors was(14.7 ±4.0)cm(range 10.2-33.0 cm).HBsAg(+)was found in 40.49% of cases.Numbers of resected segments averaged(3.3 ±1.2)in benign cases and(3.1 ±1.2)in malignant ones without significant difference between the two groups(t=1.710,P=0.310).Postoperative complications occurred in 17.29% of cases and the hospital mortality was 0.75%.The postoperative 1-,3-and 5-year survival rates in patients with malignant liver tumors were 58.3%,39.7% and 27.5%,respectively.Conclusions Hepatectomy of huge liver benign and malignant neoplasms can be performed safely with low morbidity and mortality,provided that it is carried out with skillful surgical expertise and optimized perioperative management.
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Objective To summarize the experience in surgical treatment of hepatic cavernous hemangioma (HCH). Methods The clinical data of 345 patients who received HCH resection in General Hospital of PLA from 1986 to 2005 were retrospectively analyzed. Results The ratio between male and female patients was 1/1.8. Eighteen patients (5.2%) were incidentally found with HCH during or after operation. Most of the HCH were located in the right lobe, with the proportion of 16.2% (56/345). Ninety-one patients (26.5%) had small HCH (diameter<5.0 cm), 173 (50.3%) had large HCH (diameter ranging from 5.0-10.0 cm), and 80 (23.2%) had giant HCH (diameter>10.0 cm). The mean diameter of the HCH was (8.0±5.0) cm. Three hundred and twenty-three (99.7%) patients were with Child pugh A. Right subcostal incision and enucleation were performed on all patients. The incidence of postoperative complications and mortality were 11.3% (39/345) and 0.3% (1/345), respectively. Caudate lobe resection was performed on 9 of 11 patients with the tumor located in caudate lobe. Conclusions Some HCHs may be easy to be misdiagnosed as hepatic solid tumor. HCH resection (inclu-ding hepatic caudate lobectomy) is safe for patients with HCH, and the most severe operative complication is massive bleeding during hepatectomy.
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Hypermethylation in the promoter region is an important epigenetic mechanism for the transcriptional repression of a number of cancer-associated genes, and over-expression and/or increased activity of DNA methyltransferases are considered to be the main cause of promoter hypermethylation. In order to explore the roles of two methyltransferase members (DNMT1 and DNMT3b) in the cholangiocarcinoma tumorigenesis, antisense eukaryotic expression plasmid of DNMT1 and DNMT3b gene was constructed respectively, and were co-transfected into the human cholangiocarcinoma cell line QBC-939 to observe their biological effects on the cell growth and proliferation ability, apoptosis, cell cycle alteration, and the tumorigenesis ability in the subcutaneous tissue of nude mouse. The results demonstrated that co-transfection with antisense eukaryotic expression plasmid of DNMT1 and DNMT3b gene and single transfection with antisense eukaryotic expression plasmid of DNMT1 gene can suppress the growth and proliferation of QBC-939, block the cell cycle at G1 phase, increase the apoptosis rate, minimize the tumor size in the subcutaneous tissue of nude mouse. The suppressing biological effect of co-transfection is stronger than single transfection with antisense DNMT1. Meanwhile, single transfection with antisense eukaryotic expression plasmid of DNMT3b gene has no effects on the biological characteristics of QBC-939. This study suggests that DNMT1 gene plays a key role in DNA methylation and DNMT3b gene may act as an accessory to support its function in inactivation of tumor suppressor genes. Combination DNMT1 and DNMT3b will increase their biological effects and have the synergistic effect on suppressing the growth of human cholangiocarcinoma cell line QBC-939.
Subject(s)
Apoptosis , Biliary Tract Neoplasms/metabolism , Cell Line, Tumor , Cell Proliferation , Cholangiocarcinoma/metabolism , DNA (Cytosine-5-)-Methyltransferases/biosynthesis , DNA (Cytosine-5-)-Methyltransferases/genetics , Down-Regulation , Gene Expression Regulation, Neoplastic , Genetic Vectors , Mice, Nude , Neoplasm TransplantationABSTRACT
Hypermethylation of the promoter region is an important mean for the transcriptional repression of a number of cancer-associated genes, and over-expression and/or increased activity of DNA methyltransferase are considered to be the main cause of promoter hypermethylation. In order to further explore the epigenetic mechanism of tumor suppressor gene RASSF1A inactivation, 5-aza-2'-deoxycytidine (5-Aza-CdR), a DNA methyltransferase inhibitor, was used to treat the human biliary tract carcinoma cell line QBC-939 at the concentration of 5 micromol/L for 24 h in this study. After the chemical intervention with 5-Aza-CdR, the methylation status in the promoter region of RASSF1A gene was detected by methylation specific PCR (MS-PCR), and the expression alteration of RASSF1A mRNA and protein were observed by RT-PCR and Western Blot respectively. Following the treatment with 5-Aza-CdR, methylation status in the promoter region of RASSF1A gene was reversed from methylation to unmethylation. A 280 bp DNA band which represented RASS1FA expression at transcriptional level and a 40 kDa (1 kDa=0.9921 ku) protein band which represented RASSF1A expression at protein level were detected by RT-PCR and Western Blot respectively in the experimental group cells and there were no corresponding bands in the control group cells. The experimental results suggest that 5-Aza-CdR can induce demethylation in the promoter region of RASSF1A. It can also reverse epigenetic transcriptional silencing caused by DNA methylation and induce the re-expression of RASSF1A in QBC-939. This study also suggest that the mechanism of RASSF1A inactivation is very closely related to the methylation of the promoter region, which may provide a new epigenetic understanding for tumor related gene inactivation and the pathogenesis of biliary tract carcinoma.
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Hypermethylation of the promoter region is an important mean for the transcriptional repression of a number of cancer-associated genes, and over-expression and/or increased activity of DNA methyltransferase are considered to be the main cause of promoter hypermethylation. In order to further explore the epigenetic mechanism of tumor suppressor gene RASSF1A inactivation,5-aza-2'-deoxycytidine (5-Aza-CdR), a DNA methyltransferase inhibitor, was used to treat the human biliary tract carcinoma cell line QBC-939 at the concentration of 5 μmol/L for 24 h in this study. After the chemical intervention with 5-Aza-CdR, the methylation status in the promoter region of RASSF1A gene was detected by methylation specific PCR (MS-PCR), and the expression alteration of RASSF1A mRNA and protein were observed by RT-PCR and Western Blot respectively. Following the treatment with 5-Aza-CdR, methylaiton status in the promoter region of RASSF1A gene was reversed from methylation to unmethylation. A 280 bp DNA band which represented RASS1FA expression at transcriptional level and a 40 kDa (1kDa=0.9921 ku) protein band which represented RASSF1A expression at protein level were detected by RT-PCR and Western Blot respectively in the experimental group cells and there were no corresponding bands in the control group cells. The experimental results suggest that 5-Aza-CdR can induce demethylation in the promoter region of RASSF1A. It can also reverse epigenetic transcriptional silencing caused by DNA methylation and induce the re-expression of RASSF1A in QBC-939. This study also suggest that the mechanism of RASSF1A inactivation is very closely related to the methylation of the promoter region, which may provide a new epigenetic understanding for tumor related gene inactivation and the pathogenesis of biliary tract carcinoma.
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Hypermethylation of the promoter region is one of the major mechanism of tumor suppressor gene inactivation. In order to provide a research tool for the study on the function of MBD1 gene in DNA methylation and tumorigenesis, antisense MBD1 gene eukaryotic expression plasmid was constructed and transfected into human biliary tract carcinoma cell line QBC-939 to observe its effect on the expression of MBD1 mRNA and protein by using RT-PCR and FCM respectively. Following the transfection, the mRNA level of MBD1 gene decreased from 0. 912 +/- 0.022 to 0.215 +/- 0. 017, and the protein level of MBD1 gene also decreased from (80.19 +/- 5.05) % to (35.11 +/- 4.05) %. There were very significant differences in the expression both at the transcription and post-transcription levels of MBD1 gene between non-tranfection group and the antisense MBD1 gene eukaryotic expression plasmid transfection group (P < 0.01). It was suggested that transfection with the antisense MBD1 gene eukaryotic expression plasmid can significantly reduce the expression level of MBD1 gene in QBC-939, and this study may provide a valid tool for the investigation of the function of MBD1 gene and its role in biliary tract carcinoma.
Subject(s)
Biliary Tract Neoplasms/metabolism , Biliary Tract Neoplasms/pathology , Cell Line, Tumor , DNA Methylation , DNA-Binding Proteins/biosynthesis , DNA-Binding Proteins/genetics , Eukaryotic Cells/metabolism , Gene Expression Regulation, Neoplastic , Genetic Vectors , Oligonucleotides, Antisense/genetics , Plasmids/genetics , Transcription Factors/biosynthesis , Transcription Factors/genetics , TransfectionABSTRACT
Hypermethylation of the promoter region is one of the major mechanism of tumor suppressor gene inactivation. In order to provide a research tool for the study on the function of MBD1gene in DNA methylation and tumorigenesis, antisense MBD1 gene eukaryotic expression plasmid was constructed and transfected into human biliary tract carcinoma cell line QBC-939 to observe its effect on the expression of MBD1 mRNA and protein by using RT-PCR and FCM respectively. Following the transfection, the mRNA level of MBD1 gene decreased from 0. 912±0. 022 to 0. 215±0.017, and the protein level of MBD1 gene also decreased from (80.19±5.05) % to (35.11±4.05)%. There were very significant differences in the expression both at the transcription and post-transcription levels of MBD1 gene between non-tranfection group and the antisense MBD1 gene eukary otic expression plasmid transfection group (P＜0.01). It was suggested that transfection with the antisense MBD1 gene eukaryotic expression plasmid can significantly reduce the expression level of MBD1 gene in QBC-939, and this study may provide a valid tool for the investigation of the function of MBD1 gene and its role in biliary tract carcinoma.
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Objective To study the effect of transfection of antisense MBD1 gene eukaryotic expression vector on the expression of MBD1 gene in human cholangiocarcinoma cell line QBC-939.Methods The(constructed) antisense MBD1 gene eukaryotic expression vector was transfected into the human(cholangiocarcinoma) cell line QBC-939 using lipofectamine transfection reagents,and positive cell clones were obtained using G418 selection after transfection.The constructed recombinant vector was transfected into(QBC-939) cells successfully and was confirmed by amplifying the exogenous neo~R gene with PCR method.The expression level of MBD1 gene mRNA and protein was detected by RT-PCR and FCM methods respectively.Results Following the transfection,the MBD1 gene mRNA level in human cholangiocarcinoma cell line QBC-939 decreased from 0.912?0.022 to 0.215?0.017,and the MBD1 gene protein level also(decreased) from(80.19?5.05)% to(35.11?4.05)%.There were very significant differences on the expression both at the transcription and post-transcription levels of MBD1 gene between non-tranfection group and the antisense MBD1 gene eukaryotic expression vector transfection group(P
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Objective To study the action of death signal receptor pathway of apoptosis in the development of gallbladder carcinoma . Methods Streptavidin biotin peroxidase immunohistochemistry technique was used to study the expression of Fas L in gallbladder carcinoma tissues,and TUNEL method for in situ detection of the number of apoptotic infiltrating lymphocytes around the tumor. Results The positive rates of Fas L in gallbladder carcinoma , gallbladder adenoma, dysplasia of gallbladder epithelium and chronic cholecystis were 84.6%(22/26), 83.3%(15/18) ,100%(3/3) and 55%(11/20), respectively. The positive rate of Fas L in gallbladder carcinoma was significantly higher than in chronic cholecystis (P
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Objective To explore the regulating mechanism of inducible nitric oxide synthase(iNOS) in hepatic injury of obstructive jaundice (OJ) in vivo and in vitro experiments. Methods (1) Rat hepatocytes were isolated by in situ collagenase perfusion and primary culture. Hepatocytes were pretreated with various concentrations of iNOS inhibitor SMT for 20 min. After pretreatment, 50?M GCDC was added for an additional 24hr. Cells were next detected by FCM and TUNEL.(2) Experimental obstructive jaundice (BDL) was induced by double ligation of the bile duct in rats. After BDL for 3d、7d、14d、and 21d, the apoptotic status in liver of all rats were determined with TUNEL, and iNOS protein in liver of OJ was ditermined with immunohistochemistry method. Results (1) SMT decreased GCDC-induced apoptosis in a concentration-dependent manner. (2) The apoptotic rate of liver was related to length of time of OJ. Apoptosis index (AI) was highest from rats with 14d bile duct ligation. The stronger the iNOS expression, the higher was the number of apoptotic cells that was found in OJ. Conclusions iNOS is involved in the regulation and the occurrence and progression of hepatic injury of obstructive jaundice.
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Objective To investigate the effects of the tumor suppressor gene PTEN in growing inhibition and down-regulating mTOR in cholangiocarcinoma QBC939 cells in vitro.Methods QBC939 cells were transfected with plasmids wild-type PTEN and C124S-PTEN in vitro.After transfection,the expression of the PTEN and phosphorylation of AKT and mTOR was detected by Western blot.Flow cytometry was used to analyze apoptosis and cell cycle of the transfected cells.Results Compared with the control,the expression of phosphorylation AKT was decreased and mTOR were down-regulated respectively when transfected with the wild-type PTEN.However,after transfection with mutation-type PTEN,the level of PTEN in the cells by increased,but phosphorylation AKT level and mTOR expression had no significant change.Conclusions PTEN can be actived by phosphorylated AKT.Actived AKT decreased the mTOR which led to tumor cells apoptosis and regulation of the tumor cell cycle.In the pathway of signal transmission of PI3K/AKT/PTEN/mTOR,PTEN and mTOR are closely related through phosphorylation of AKT.