Biomedical subjects

Cheng-Chung Wu

Publications and source records attributed to Cheng-Chung Wu.

At least 19 recordsLinked to original sources

PubMed2006

Elevated plasma osteopontin associated with gastric cancer development, invasion and survival.

OBJECTIVE: Osteopontin (OPN) has been found to be valuable in diagnosis and predicting the prognosis of a variety of malignancies. The aims of the present study are to evaluate the usefulness of plasma OPN level for predicting gastric cancer development, invasion and survival. PATIENTS AND METHODS: One hundred and thirty two gastric cancer patients and 93 healthy controls were enrolled. Real-time quantitative reverse-transcription polymerase chain reaction and immunohistochemical staining were used to detect OPN expression in gastric cancer tissues. Plasma levels of OPN were measured by enzyme-linked immunosorbent assay. Plasma OPN levels were compared with gastric cancer development, clinicopathological features and outcomes. RESULTS: Expression of OPN mRNA was significantly higher in gastric cancer tissues compared with non-tumour tissues. Most OPN immunoactivity was localised to cancer cells. The median plasma OPN level was significantly higher in patients than in controls (p<0.0001), and significantly higher in patients with advanced stages, serosal invasion, lymph node metastasis, lymphatic invasion, venous invasion and liver metastasis. Logistic regression showed that high plasma OPN level (greater than 67.3 ng/ml) is significantly associated with advanced stages, serosal invasion, lymph node metastasis, lymphatic invasion, venous invasion and liver metastasis. Plasma OPN level demonstrated significant association with patient survival (p<0.0001), especially in the subgroups with invasive phenotypes. On Cox multivariate analysis, elevated plasma OPN level was an independent risk factor for poor survival (p<0.0001). CONCLUSIONS: Elevated plasma OPN level is significantly associated with gastric cancer development, invasive phenotypes and survival. Plasma OPN level may have potential usefulness as a diagnostic and prognostic factor for gastric cancer.

Adenocarcinoma↗

PubMed2006

Overexpression of anion exchanger 2 in human hepatocellular carcinoma.

To compare gene expression patterns between the poorly-differentiated (HA22T/VGH) and well-differentiated (HepG2) hepatocellular carcinoma cells, messenger RNA was isolated form both kinds of cells and subjected to differential displays reversing transcriptase-polymerase chain reaction (DDRT-PCR) technology. Gene fragments showing difference in the expression were recovered, reamplified, cloned and sequenced. Anion exchanger 2 (AE2), an isoform of band 3 protein, was identified and chosen for further characterization. AE2 was strongly expressed in HA22T/VGH cells, while it was little expressed in the well-differentiated hepatocellular carcinoma cells (PLC/PRF5 and HepG2) or little in the normal liver cell (Chang liver). In the 28 pairs of HCC and adjacent non-tumor tissues, levels in the cancer tissue (32.7 +/- 5.0) were significantly higher than that in the adjacent non-tumor tissue (9.1 +/- 2.4) (P < 0.01). Moreover, 19 cases (68%) showed over-expression of AE2 in HCC tissues, 3 cases were similar in both tissues, and 6 cases exhibited little or undetectable signals. Twenty cases (71%) of adjacent normal tissue showed little or undetectable signals. The results indicated that overexpression of AE2 may be involved in the development of human HCC.

Aged↗

PubMed2006

Apoptotic and anti-proliferative effects of 17beta-estradiol and 17beta-estradiol-like compounds in the Hep3B cell line.

Since there is evidence for estrogen and estrogen-like compounds to have beneficial effect on the pathogenesis of hepatocellular carcinoma (HCC), this study was designed to investigative the apoptotic and anti-proliferative effects of these compounds on the human hepatoma Hep3B cell line. The Hep3B cells were treated with 17beta-estradiol (E2), diethylstilbestrol (DES), tamoxifen, and genistein. After treatments of these compounds at the concentration of 10(-6) or 10(-8) M, the Hep3B cells were demonstrated to have significant DNA fragmentation, nucleus condensation, cytochrome-c leaking from the mitochondria and caspase-3 activation by DAPI and Western blotting. The cells were also observed to have declined proliferative potential by MTT assay, arrested cell cycle by flow-cytometry measurements. However, the cytochrome-c leaking from the mitochondria induced by E2 and E2-like compounds was blocked totally by ICI 182,780 treatment. These finding suggest that estrogen and the estrogen-like compounds may induce anti-proliferative and apoptotic effects in Hep3B cells, and the E2 and the E2-like compounds mediated apoptotic effect was estrogen receptor dependent. Among the drugs tested, E2, E2 agonists (DES and genistein) and partial antagonist (tamoxifen), all showed the stronger anti-tumor potential.

Apoptosis↗

PubMed2006

Apoptotic effects of over-expressed estrogen receptor-beta on LoVo colon cancer cell is mediated by p53 signalings in a ligand-dependent manner.

Epidemiologic studies reported that the prevalence of hereditary non-polyposis colon cancer (HNPCC) in male is about 1.5-fold higher than that in female. Decreases in circulatory estradiol (E2) have been reported to downregulate the expression of E2 receptor (ER) and significantly increase the risk of colorectal cancer. Patients that received E2 replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma. Furthermore, significant decreases in the expression of ER have been found in colorectal cancer specimens. These data strongly suggest the protective roles of E2 and ER against colorectal cancer. However, the mechanisms remain unexplored. LoVo cells were transient transfected to overexpress ER-beta, DNA fragmentation and caspase activity assay were performed to evaluate apoptotic effects. Western blotting was used to evaluate protein levels, and luciferase activity assay to measure the TNF-alpha promoter activity. Our data clearly demonstrated that E2 and ER-beta alone could upregulate p21 and p27 proteins, which further activate caspase-8 and caspase-9 to induce apoptosis in LoVo cell, and the ER-beta. effects were enhanced by E2. However, overexpressed ER-beta did not influence the expression and promoter activity of TNF-alpha. In addition, E2 and overexpressed ER-beta downregulated the beta-catenin proteins which cause the downregulation of its target genes, cyclin D1 and Rb, to inhibit the cell cycle and cell proliferation. The results indicate that overexpressed ER-beta may induce LoVo cell apoptosis and anti-proliferation by increasing p53 signaling in a ligand-dependent manner, and without hTNF-alpha involvement. Efforts aiming at enhancing ER-beta expression and/or activity may prove to be an attractive alternative therapy against colorectal cancer.

Apoptosis↗

PubMed2006

Opposing action of estrogen receptors alpha and beta on tumor necrosis factor-alpha gene expression and caspase-8-mediated apoptotic effects in HA22T cells.

Hepatocellular carcinoma (HCC), the major manifestation of primary liver cancer, is one of the most frequent and malignant cancers worldwide, especially in Taiwan. Estrogen receptors (ERs) have been reported to play either a proliferation- or apoptosis-enhancing role in the differentiation of cancers, including HCC. In a previous experiment, we showed that transient overexpressed estrogen receptor-alpha induced early stage HCC cell line Hep 3B cell apoptosis by increasing the hTNF-alpha gene expression in a ligand-independent manner. To further clarify if the apoptotic effect occurs in poorly differentiated HCC cell line, HA22T, and elucidate the roles of ERs and TNF-alpha, DNA fragmentation and caspase activity were measured in late stage HCC cell line, HA22T, by measuring the expression of hER-alpha and hER-beta using a Tetracycline-inducible system (Tet-on). Increased DNA fragmentation and caspase-3 activity were found in hERbeta-overexpressed HA22T cells treated with estrogen (10(-8) M) but not in hERalpha-overexpressed HA22T cells. Using RT-PCR/PCR and western blotting in HA22T cells, overexpressed hER-beta was also found to increase the expression of hTNF-alpha mRNA and induce hTNF-alpha-dependent luciferase activity in a ligand-dependent manner. Additionally, LPS treatment and hER-beta overexpression both enhance caspase-8 activities, whereas neither hER-beta nor E2 treatment affected caspase-9 activities. In addition, the overexpressed hER-beta plus E2 enhanced DNA fragmentation and caspase-8 activities were only partially reduced by anti-hTNF-alpha (0.1 ng/ml), which was possibly due to the involvement of P53 and TGF-beta. Taken together, our data indicates that overexpressed hER-beta but not hER-alpha may induce caspase-8-mediated apoptosis by increasing the hTNF-alpha gene expression in a ligand-dependent manner in poorly differentiated HA22T cells.

Apoptosis↗

PubMed2006

Liver resection for hepatocellular carcinoma in patients who have undergone prior renal transplantation.

BACKGROUND AND OBJECTIVES: Because renal transplantation recipients require immunosuppressive drugs, they have a higher incidence of subsequent malignancies. Among them, hepatocellular carcinoma (HCC) is common. Although liver resection remains an option for curing HCC, the role of liver resection in renal transplantation recipients remains unclear. METHODS: A retrospective review of liver resection for newly diagnosed HCC in 680 patients was conducted. Among them, 18 patients had undergone prior renal transplantation (RT group). The patient background, tumor characteristics, early and long-term results after liver resection were compared with the other 662 patients who had not previously undergone renal transplantation (non-RT group). RESULTS: The patient's background characteristics were comparable between RT and non-RT group. The tumor characteristics, postoperative morbidity, and mortality were not significantly different between the two groups. The 5-year disease-free survival rates in RT and non-RT groups were 18.8% and 41.2%, respectively (P = 0.242), whereas 5-year actuarial survival rates in RT and non-RT groups were 59.1% and 58.3%, respectively (P = 0.738). Two patients lost their graft kidney 3 and 8 years after liver resection. CONCLUSION: With careful protection of the graft kidney, liver resection is still a justified treatment option for HCC in patients who have undergone renal transplantation.

Abdominal Abscess↗

PubMed2006

Large cell neuroendocrine carcinoma of the ampulla of vater: Report of a case.

Large cell neuroendocrine carcinoma in the ampulla of Vater is rare and very different from the common ampullary adenocarcinoma. A 59-year-old man was admitted with obstructive jaundice. Gastroendoscopy showed a swollen ampulla of Vater and pathological examination of an ampullary biopsy revealed findings of a carcinoid tumor. After endoscopic biliary drainage, he underwent pancreaticoduodenectomy. A diagnosis of large cell neuroendocrine carcinoma was confirmed by immunohistochemical examination of the resected specimen. Despite adjuvant chemotherapy with cyclophosphamide and cisplatin, liver and peritoneal metastasis developed within 5 months and he survived for only 10 months after the operation. Thus, further investigations are needed to find a more effective postoperative adjuvant chemotherapy agent to treat patients with this aggressive tumor.

Ampulla of Vater↗

PubMed2006

Role of glucocorticoid receptor in serosa-involved gastric carcinoma after gastrectomy.

Glucocorticoid receptor (GR) was first found in the cytosol of gastric cancer tissue more than 15 years ago. At present, most gastric cancers are diagnosed at the advanced stage. To elucidate the role of GR in gastric cancer, the GR levels of the cancer tissue of 75 consecutive patients with grossly serosa-involved gastric carcinoma were determined by the dextran-coated charcoal method. The clinicopathologic characteristics and long-term survival duration were compared in patients with GR-positive and GR-negative cancer cells. We found that GR could be detected in the cytosol of cancer cells in 31 (41.3%) of the gastric cancer patients with a median concentration of 18.5 (range, 1.03-73.9) fmol/mg protein. No significant differences could be found in any clinicopathologic characteristic between the patients with GR-positive and GR-negative cancers. After multivariate analysis, gross Borrmann's type, metastatic lymph node number, and GR positivity were the independent prognostic factors after gastrectomy for serosa-involved gastric carcinoma. GR-positive gastric cancer had a worse survival rate than GR-negative gastric cancer. Multimodality adjuvant therapies should be considered in patients with GR-positive serosa-involved gastric carcinoma.

Adult↗

PubMed2006

Perioperative parenteral tranexamic acid in liver tumor resection: a prospective randomized trial toward a "blood transfusion"-free hepatectomy.

OBJECTIVE: To examine the feasibility of a real "blood transfusion"-free hepatectomy in a large group of patients with liver tumors. SUMMARY BACKGROUND DATA: Bleeding control and blood transfusion remains problematic in liver resection. A real "blood transfusion"-free hepatectomy in a large group of patients has rarely been reported. The impact of tranexamic acid (TA), an antifibrinolytic agent, on blood transfusion in liver resection is unknown. METHODS: A prospective double-blind randomized trial was performed on elective liver tumor resections. In group A, TA 500 mg was intravenously administered just before operation followed by 250 mg, every 6 hours, for 3 days. In group B, only placebo was given. The patients' background, blood transfusion rates, and early postoperative results in the 2 groups were compared. Factors that influenced blood requirement were analyzed. RESULTS: There were 108 hepatectomies in group A and 106 hepatectomies in group B. The patients' backgrounds, operative procedures, and hepatectomy extent did not significantly differ between the 2 groups. Although the differences of the operative morbidity and postoperative stay were not significant, a significantly lower amount of operative blood loss, lower blood transfusion rate, shorter operative time, and lower hospital costs were found in group A patients. No patient in group A received blood transfusion. No hospital mortality occurred in either group. Tumor size and use of TA were independent factors that influenced blood transfusion. CONCLUSIONS: Perioperative parenteral use of TA reduced the amount of operative blood loss and the need for blood transfusion in elective liver tumor resection. A real "blood transfusion"-free hepatectomy may be feasible with the assistance of parenteral TA.

Aged↗

PubMed2006

Porphyromonas gingivalis-related cardiac cell apoptosis was majorly co-activated by p38 and extracellular signal-regulated kinase pathways.

BACKGROUND AND OBJECTIVE: Little is known about the pathogenesis of apoptosis caused in cardiac tissues by periodontitis pathogens. The purpose of this study was to determine the related effect of periodontal pathogen Porphyromonas gingivalis on cardiac cell apoptosis. METHODS: DNA fragmentation, nuclear condensation and activated apoptotic caspases were measured by agarose gel electrophoresis, nuclear DAPI (4',6-diamidine-2-phenylindole dihydrochloride) stain and western blotting analysis following the surrounding medium of P. gingivalis and/or pre-administration of SB203580 (p38 inhibitor), U0126 [mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor], LY294002 [phosphoinositide 3-kinase (PI3K) inhibitor], cyclosporine A (CsA: calcineurin inhibitor), and Sp600125 [c-Jun N-terminal kinase (JNK) inhibitor] in cultured cardiac H9c2 cells. RESULTS: The surrounding medium of periodontal pathogen P. gingivalis increased DNA fragmentation, nuclear condensation and the activated apoptotic caspase-3, -8, and -9 proteins in H9c2 cells. DNA fragmentation and nuclear condensation of H9c2 cells treated with P. gingivalis medium were completely blocked by SB203580 plus U0126 and were decreased after pre-administration of SB203580 only, U0126 only, LY294002, CsA, but were increased by Sp600125. CONCLUSION: Our findings suggest that the development of cardiac cell apoptosis can be directly induced by P. gingivalis medium. Porphyromonas gingivalis-related H9c2 cell apoptosis was mainly co-activated by p38 and ERK pathways and may be involved in death receptor-dependent (caspase 8) and mitochondria (caspase 9)-dependent apoptotic pathways. Porphyromonas gingivalis-related cardiac cell apoptosis was also partially mediated by PI3K or calcineurin signaling pathways, whereas the JNK pathway might play a protective role in P. gingivalis-related cardiac cell apoptosis.

Animals↗

PubMed2006

Porphyromonas gingivalis-induced cellular hypertrophy and MMP-9 activity via different signaling pathways in H9c2 cardiomyoblast cells.

BACKGROUND: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy. METHODS: Matrix metalloproteinase (MMP)-2 and MMP-9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis-medium treatment with or without SB203580 (p38 mitogen-activated protein kinase cascade [p38] inhibitor), U0126 (mitogen-activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3-kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)-1, or anti-inflammatory IL-10 in cultured cardiomyoblast H9c2 cells. RESULTS: P. gingivalis medium increased MMP-9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP-9 treated with P. gingivalis medium was not mediated through p38, extracellular-regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL-10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (-37%), U0126 (-35%), LY294002 (-49%), CsA (-49%), and SP600125 (-24%). CONCLUSIONS: Our findings suggest that P. gingivalis medium elevated MMP-9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis-induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis-elevated MMP-9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

Calcineurin↗

PubMed2005

Mitochondrial genome instability and mtDNA depletion in human cancers.

An increase in the rate of glycolysis is one of the metabolic alterations in most cancer cells. However, the role of alterations in mitochondrial function and mitochondrial DNA (mtDNA) in carcinogenesis still remains unclear. In this study, we analyzed the nucleotide sequence of the D-loop and the copy number of mtDNA in 54 hepatocellular carcinomas (HCCs), 31 gastric, 31 lung, and 25 colorectal cancers as well as their corresponding non-tumorous tissues. The results revealed that 42.6% (23/54) of the HCCs, 51.6% (16/31) of the gastric cancers, 22.6% (7/31) of the lung cancers, and 40.0% (10/25) of the colorectal cancers harbored mutation(s) in the D-loop of mtDNA. The mtDNA mutations in 43.5% (10/23) of the HCCs, 62.5% (10/16) of the gastric cancers, 57.1% (4/7) of the lung cancers, and 90.0% (9/10) of the colorectal cancers were changes in the mononucleotide or dinucleotide repeats, deletions, or multiple insertions. Moreover, we found that there is a significant decrease in mtDNA copy number in 57.4% (31/54) of the HCCs, 54.8% (17/31) of the gastric cancers, 22.6% (7/31) of the lung cancers, and 28.0% (7/25) of the colorectal cancers compared with the corresponding non-tumorous tissues. It is noteworthy that the incidence of somatic mutations in the D-loop of mtDNA in the cancers of later stages was higher than that of the early-stage cancers. Taken together, our findings suggest that instability in the D-loop region of mtDNA, together with the decrease in mtDNA copy number, is involved in the carcinogenesis of human cancers.

DNA, Mitochondrial↗

PubMed2004

Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor kappaB expression and enhanced antiapoptosis-related proteins in Helicobacter pylori-infected non-cardiac gastric adenocarcinoma.

AIM: Several epidemiological studies have demonstrated a close association between Helicobacter pylori (H pylori) infection and non-cardiac carcinoma of the stomach. H pylori infection induces active inflammation with neutrophilic infiltrations as well as production of oxygen free radicals that can cause DNA damage. The DNA damage induced by oxygen free radicals could have very harmful consequences, leading to gene modifications that are potentially mutagenic and/or carcinogenic. The aims of the present study were to assess the effect of H pylori infection on the expression of inducible nitric oxidative synthase (iNOS) and the production of 8-hydroxy-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury in human gastric mucosa with and without tumor lesions, and to assess the possible factors affecting cell death signaling due to oxidative DNA damage. METHODS: In this study, 40 gastric carcinoma specimens and adjacent specimens were obtained from surgical resection. We determined the level of 8-OHdG formation by HPLC-ECD, and the expression of iNOS and mechanism of cell death signaling (including nuclear factor-kappaB(NFkappaB), MEKK-1, Caspase 3, B Cell lymphomal leukemia-2 (Bcl-2), inhibitor of apoptosis protein (IAP) and myeloid cell leukemia-1 (Mcl-1)) by Western-blot assay. RESULTS: The concentrations of 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP were significantly higher in cancer tissues than in adjacent non-cancer tissues. In addition, significantly higher concentrations of 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP were detected in patients infected with H pylori compared with patients who were not infected with H pylori. Furthermore, 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP concentrations were significantly higher in stage 3 and 4 patients than in stage 1 and 2 patients. CONCLUSION: Chronic H pylori infection induces iNOS expression and subsequent DNA damage as well as enhances anti-apoptosis signal transduction. This sequence of events supports the hypothesis that oxygen-free radical-mediated damage due to H pylori plays a pivotal role in the development of gastric carcinoma in patients with chronic gastritis.

Adenocarcinoma↗

PubMed2004

Somatic mutations in the D-loop and decrease in the copy number of mitochondrial DNA in human hepatocellular carcinoma.

Somatic mutations in mitochondrial DNA (mtDNA) have been detected in many human cancers, including hepatocellular carcinoma (HCC). The D-loop region was found to be a "hot spot" for mutation in mtDNA of the tumors. However, effects of the D-loop mutations on the copy number of mtDNA in tumor tissues are poorly understood. Using direct sequencing, we examined mutations in the D-loop region of mtDNA in 61 HCCs and the corresponding non-tumor liver tissues. The results revealed that 39.3% of the HCCs carried somatic mutation(s) in the D-loop of mtDNA, and most of these mutations were homoplasmic. Moreover, 37.0% (10/27) of these mutations were T-to-C and G-to-A transitions and 40.7% (11/27) of them were located in the polycytidine stretch between nucleotide position (np) 303 and 309 of mtDNA. In addition, we found that mtDNA copy number of HCC was significantly decreased in 60.5% of the patients with hepatoma, especially in those with somatic mutation(s) in the D-loop of mtDNA (17/24). This decrease in mtDNA copy number was highly associated with the occurrence of point mutations near the replication origin of the heavy-strand of mtDNA. Interestingly, we found that 42.9% (6/14) of the HCCs without mutation in the D-loop had a reduced copy number of mtDNA, indicating that other unidentified factors involved in mitochondrial biogenesis might be defective in the tumor. The results obtained in this study strongly suggest that somatic mutations in the D-loop together with the decrease in the copy number of mtDNA may be an important event during the early phase of liver carcinogenesis.

Base Sequence↗

PubMed2004

Small bowel obstruction caused by a congenital intestinal web with an enteric bezoar in an adult: report of a case.

An intestinal web is a rare congenital anomaly, typically reported in childhood, but often remaining asymptomatic throughout the entire life span of the individual. We report the case of a symptomatic intestinal web associated with an enteric bezoar in an adult, which to the best of our knowledge has never been documented before. A 25-year-old man presented with acute small bowel obstruction, and laparotomy revealed a stenotic area of the ileum as well as impaction of an enteric bezoar. We resected this segment of ileum and an intestinal web was subsequently found in the stenotic area. The patient recovered well and has remained asymptomatic for 3 years. Although rare, a congenital intestinal web may be a cause of adult small bowel obstruction requiring surgical resection.

Adult↗

PubMed2004

Appraisal of concomitant splenectomy in liver resection for hepatocellular carcinoma in cirrhotic patients with hypersplenic thrombocytopenia.

BACKGROUND: Liver resection usually is not recommended for hepatocellular carcinoma (HCC) in cirrhotic patients with portal hypertension. The role of concomitant splenectomy in liver resection for HCC in cirrhotic patients with hypersplenic thrombocytopenia (HT) resulting from portal hypertension remains undefined. METHODS: Among 526 cirrhotic patients who underwent liver resection for HCC, 41 underwent a concomitant splenectomy (Sp group) because of HT (platelet count </=80 x 10(3)/mm(3)). The patients' backgrounds, pathologic characteristics of HCC, and short- and long-term results after liver resection of Sp group were compared with those of the other 485 cirrhotic patients who did not undergo splenectomy (non-Sp group). RESULTS: Compared to the non-Sp group, the liver function was worse, the tumor size was smaller, the liver resection extent was narrower, and tumor stages were earlier in the Sp group. The postoperative morbidity, mortality, hospital stay, and hospital costs were not significantly different between the groups. The disease-free survival rate of the Sp group was better than that of non-Sp group, but the actuarial survival rates of both groups were similar. After stratification with UICC-TNM stages, there were no significant differences regarding the disease-free and actuarial survival rates in each stage. CONCLUSIONS: Concomitant splenectomy extends the indication of liver resection for HCC in cirrhotic patients with portal hypertension. It is justified in selected cirrhotic patients with HCC and HT.

Aged↗

PubMed2003

Bacterial translocation after cirrhotic liver resection: a clinical investigation of 181 patients.

BACKGROUND: Cirrhotic patients are usually associated with a high susceptibility to infection. Although bacterial translocation from gut mucosa to mesenteric lymph node (MLN) and systemic circulation is a well-known phenomenon after hepatectomy, its role in cirrhotic patients remains unclear. MATERIALS AND METHODS: MLN was harvested for bacterial culture before and after liver resection in 181 cirrhotic patients. The characteristics and postoperative courses of patients with positive and negative bacterial culture for MLN after hepatectomy were compared. Postoperative systemic antibiotics were administered if infectious complications occurred. RESULTS: No bacteria were cultured in MLN before hepatectomy. Bacterial translocation (BT) to MLN after hepatectomy occurred in 36 patients (BT group). After multivariate analysis, intraoperative blood transfusion was the only independent factor that influenced bacterial translocation rates after cirrhotic liver resection. BT group patients also had higher infectious and overall complication rates, with a longer postoperative hospital stay. Among the cultured bacteriae from infected sites in BT group patients with infectious complications, only 2 patients (12.5%) had totally different bacterial species to those cultured from MLNs. CONCLUSIONS: Bacterial translocation more often occurred after liver resection in cirrhotic patients who received intraoperative blood transfusion. Such patients had higher postoperative infectious and overall complication rates. Thus, avoidance of intraoperative blood transfusion is mandatory for cirrhotic liver resection.

Bacterial Infections↗

PubMed2003

Dominant mutations of hepatitis B virus variants in hepatoma accumulate in B-cell and T-cell epitopes of the HBx antigen.

Hepatitis B virus (HBV) X gene, encoding a pleotropic transactivator of HBx protein, has been associated with the development of hepatocellular carcinoma (HCC). Molecular information on liver-derived HBV variants isolated from HCC among Taiwanese population was studied. Amplification of the HBV X genes of 20 HCC patients in high stringency with HBV specific primers was observed. The resulting amplified HBV X genes were purified and individually-cloned into pUC-T vector. Sequences of the eight liver-derived X gene were aligned and compared with the wild type, the ayw HBV serotype. Results indicate that the HBx protein of variants were found predominantly within the regions of amino acid positions 26-45 in N-terminus, and positions 87, 88, 116, 118, 119, 127 and 144. Sequences from six out of the eight variants were found to be identical. These accumulated sequence mutations among the eight HBx variants were found to coincide within the B-cell epitopes (positions 29-48), particularly in the HBx proline and serine rich (PSR) domain, and the T-cell epitopes regions (positions 116-127). These frequent mutations of HBV variants, rather than subtype-specific polymorphic sites, may be involved in immunoevasion.

Amino Acid Sequence↗