Cystic lymphangioma of the chest wall: a case report.

Cystic lymphangioma is a congenital cystic malformation that occurs mostly in children. While it is mainly found in the cervix, cases in the chest wall are very rare. We report a case of cystic lymphangioma found in the chest wall of a 2-month-old girl. The patient was noted to have a tumor in the left chest wall at birth. Since it gradually increased in size, the patient was referred to our department. Transillumination and ultrasonography showed a cystic lesion in the left chest. Surgical resection was performed in one step. Histopathological examination showed a cystic lymphangioma.

Successful surgical control of peritoneal dissemination of hepatocellular carcinoma.

Treatment for the peritoneal dissemination of hepatocellular carcinoma (HCC) has not yet been established. We report a patient with HCC associated with disseminated intra-abdominal tumor. A 74-year-old man was admitted to our hospital. Computed tomography showed a 3 × 3 cm mass in the left hepatic lobe and a giant mass between the stomach and spleen. At laparotomy, the tumor was seen in the medial segment and evaginated to the diaphragm. There was a tumor between the stomach and spleen, confirmed as a 5 × 5 cm tumor evaginated from the left diaphragm, and a 7 × 7 cm tumor adhesive to the spleen. These two tumors were not continuous and were separated. Furthermore, we confirmed a 10 × 10 cm tumor in the pelvic cavity. We performed partial hepatectomy, resection of the tumor evaginated from the diaphragm, resection of the tumor of the spleen and tail of pancreas, and resection of the tumor in the pelvic cavity. Histopathologically, all resected tumors were confirmed to be well-differentiated HCC. HCC rarely disseminates intraperitoneally. It is considered that the peritoneal dissemination of HCC occurred from poorly differentiated or undifferentiated type. Then this report is a rare case. Although surgical treatment of peritoneal dissemination of HCC is not curative, surgery may improve survival and provide good quality of life in selected cases.

Stimulation of liver regeneration after hepatectomy in mice by injection of bone marrow mesenchymal stem cells via the portal vein.

AIM: To investigate whether mouse bone marrow mesenchymal stem cells (BMC) stimulate liver regeneration after partial hepatectomy. METHODS: Isolated BMCs were purified by density gradient centrifugation. We performed a 70% hepatectomy in male BALB/c mice followed by injection of BMCs into the portal vein (PV-BMC group), or the tail vein (IV-BMC group), or of saline into the portal vein (control group). RESULTS: The wet weight of the liver remnant increased significantly in the PV-BMC group at 3 and 5 days after hepatectomy compared with the IV-BMC and control groups. The Ki-67 labeling index revealed that the increase to result from stimulation of DNA synthesis. The constitutive interleukin-6 and hepatocyte growth factor mRNAs in the remnant liver tended to increase in the PV-BMC group at 3 days after hepatectomy. CONCLUSIONS: These results demonstrated that BMC injection into the portal vein enhanced liver growth after partial hepatectomy in mice.

Change in donor quality of life after living donor liver transplantation surgery: a single-institution experience.

AIM: Changes in quality of life (QOL) of donors after living donor liver transplantation surgery were studied using Short Form 36 (SF-36) to evaluate physical health and the Profile of Mood States (POMS) to evaluate mood. METHODS: Among the 28 donors who had undergone surgery at our hospital, 21 donors replied to our questionnaire (recovery rate: 75%). Changes in the QOL of donors were examined based on the results of pre- and postoperative SF-36 and POMS and a questionnaire survey. RESULTS: The donors included 12 men and nine women with a mean age of 43 years. One donor operation was complicated by biliary stenosis. The SF-36 results showed significant postoperative decline in physical function and increase in pain, but no other significant changes. The POMS results showed no significant differences, with the mean values for anxiety, depression, anger, vitality, and confusion all recovering postoperatively. The questionnaire results indicated that all subjects had recovered physical function, but 24% of subjects felt wound-related physical symptoms and 19% felt anxiety concerning their future health. CONCLUSIONS: Some donors had symptoms that persisted for comparatively long periods postoperatively and considered that long-term outpatient observation was required. No significant psychological changes were found, but donors felt anxiety about their future health and considered that patient meetings would be useful and that adequate outpatient health guidance should be provided.

Phase II trial of preoperative S-1 plus cisplatin followed by surgery for initially unresectable locally advanced gastric cancer.

BACKGROUND: The aim of this study was to evaluate the efficacy and feasibility of preoperative chemotherapy with S-1 plus cisplatin in patients with initially unresectable locally advanced gastric cancer. METHODS: We enrolled patients with initially unresectable locally advanced gastric cancer because of severe lymph node metastases or invasion of adjacent structures. Preoperative chemotherapy consisted of S-1 at 80 mg/m(2) divided in two daily doses for 21 days and cisplatin at 60 mg/m(2) intravenously on day 8, repeated every 35 days. If a tumor decreased in size, patients received 1 or 2 more courses. Surgery involved radical resection with D2 lymphadenectomy. RESULTS: Between December 2000 and December 2007, 27 patients were enrolled on the study. No CR was obtained, but PR was seen in 17 cases, and the response rate was 63.0%. Thirteen patients (48.1%) had R0 resections. There were no treatment related deaths. The median overall survival time (MST) and the 3-year overall survival (OS) of all patients were 31.4 months and 31.0%, respectively. Among the 13 patients who underwent curative resection, the median disease-free survival (DFS) and the 3-year DFS were 17.4 months and 23.1%, respectively. The MST and the 3-year OS were 50.1 months and 53.8%, respectively. The most common site of initial recurrence after the R0 resection was the para-aortic lymph nodes. CONCLUSIONS: Preoperative S-1 plus cisplatin can be safely delivered to patients undergoing radical gastrectomy. This regimen is promising as neoadjuvant chemotherapy for resectable gastric cancer. For initially unresectable locally advanced gastric cancer, new trials using more effective regimens along with extended lymph node dissection are necessary.

Active hexose correlated compound inhibits the expression of proinflammatory biomarker iNOS in hepatocytes.

BACKGROUND/AIMS: Excess production of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) has been implicated as proinflammatory biomarker in liver injury. The application of active hexose correlated compound (AHCC) as a functional food in complementary and alternative medicine has increased. The possibility that AHCC might inhibit iNOS induction was investigated as a potential liver-protective effect. METHODS: Hepatocytes were isolated from rats by collagenase perfusion and cultured. Primary cultured hepatocytes were treated with interleukin-1ß in the presence or absence of AHCC-sugar fraction (AHCC-SF). RESULTS AND CONCLUSION: AHCC-SF inhibited the production of NO and reduced expressions of iNOS mRNA and its protein. AHCC-SF had no effects on either IκB degradation or nuclear factor-κB (NF-κB) activation. In contrast, AHCC-SF inhibited the upregulation of type I interleukin-1 receptor (IL-1RI) through the inhibition of Akt phosphorylation. Transfection experiments with iNOS promoter-luciferase constructs revealed that AHCC-SF reduced the levels of iNOS mRNA at both promoter transactivation and mRNA stabilization steps. AHCC-SF inhibited the expression of iNOS gene antisense transcript, which is involved in iNOS mRNA stabilization. These findings demonstrate that AHCC-SF suppresses iNOS gene expression through a IκB/NF-κB-independent but Akt/IL-1RI-dependent pathway, resulting in the reduction of NO production. AHCC-SF may have therapeutic potential for various liver injuries.

Surgical Control of a Primary Hepatic Carcinoid Tumor: A Case Report.

We report a primary hepatic carcinoid tumor occurring in a 47-year-old man. The patient consulted our hospital complaining of epigastralgia. Abdominal ultrasonography, computed tomography scanning, and magnetic resonance imaging showed a large mass in the right lobe of the liver. FDG-PET revealed 18F-FDG uptake by the right hepatic lobe. The tumor was a solid mass with cystic components, approximately 15 cm in diameter. We conducted an extended right lobectomy of the liver. The resected specimen was a solid tumor with cystic components and hemorrhagic lesion. Microscopic findings showed that the tumor cells had round nuclei and formed trabecular patterns. Immunohistologically, tumor cells were stained positive for chromogranin A, neuron specific enolase, CD56, and S-100. Careful examinations before and after the operation revealed no other possible origin of the tumor. Based on these findings, the tumor was diagnosed as a primary hepatic carcinoid. This is a report of a rare case of a primary hepatic carcinoid tumor with a discussion of several other relevant reports.

Neutrophil elastase inhibitor prevents endotoxin-induced liver injury following experimental partial hepatectomy.

BACKGROUND: During endotoxaemia, neutrophils activated by inflammatory cytokines release reactive oxygen species and neutrophil elastase, resulting in hepatic necrosis and dysfunction. This study investigated the possible mechanism underlying the protective effect of sivelestat, a neutrophil elastase inhibitor, on endotoxin-induced liver injury following partial hepatectomy. METHODS: Lipopolysaccharide (LPS) was administered intravenously to male Sprague-Dawley rats 48 h after 70 per cent hepatectomy. Sivelestat or normal saline was given intravenously before LPS administration, RESULTS: Treatment with sivelestat significantly improved the survival rate. Sivelestat prevented increases in the concentration of serum enzymes and total bilirubin related to liver injury. Levels of inflammatory cytokines in serum and liver tissue were significantly lower in the sivelestat-treated group than in the control group. The degree of neutrophil infiltration, necrosis and apoptosis in the remnant liver was significantly decreased in sivelestat-treated rats. Sivelestat pretreatment inhibited the activation of nuclear factor (NF) kappaB, caspase 3 and 8 activities, and cytochrome c release. CONCLUSION: Sivelestat prevents LPS-induced liver injury by inhibition of NF-kappaB activation and apoptosis.

Enhanced production of interleukin 6 in peripheral blood monocytes stimulated with mucins secreted into the bloodstream.

PURPOSE: It has been reported that tumor progression is correlated with the serum level of interleukin 6 (IL-6). The purpose of this study was to investigate by what mechanism, other than production from tumor cell, the serum level of IL-6 is elevated in the tumor-bearing state. EXPERIMENTAL DESIGN: Monocytes from healthy donors were cultured in the presence of sera from colon cancer patients, and the activity to elevate IL-6 production was estimated. This activity of serum was also examined after various biochemical treatments. RESULTS: When monocytes from healthy donors were cultured in the presence of sera from patients with colon cancer, secretion of IL-6 from the cells was markedly elevated. Serum proteins were fractionated on Sepharose 4B and the activity to elevate IL-6 production was found in the excluded fractions. Sialyl Tn antigen was detected in these same fractions. By excluding some mucins from the serum, the inducing activity was reduced to 40% of the original level. Furthermore, we purified mucins from the conditioned medium of colon cancer cells. Production of IL-6 was effectively elevated by a small amount of purified mucins in a dose-dependent manner. When the inducing activity was examined in the presence of binding or competitive inhibitors to the scavenger receptor, the effect was remarkably reduced. CONCLUSIONS: Mucins secreted from colon cancer cells into the bloodstream induce production of IL-6 in peripheral blood monocytes through the scavenger receptor, which may be responsible for the high level of serum IL-6 in colon cancer patients.

Protective effect of fibronectin for endotoxin-induced liver injury after partial hepatectomy in rats.

BACKGROUND: Endotoxemia may occur after hepatectomy and become the cause of post-operative death. Fibronectins (Fns) are involved in a number of biological processes, such as cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, and ischemic injury. Studies were performed to determine whether Fn influences the survival rate of rats subjected to endotoxin-induced liver injury after partial hepatectomy. MATERIALS AND METHODS: Lipopolysaccharide (LPS) was administered intravenously to male Sprague-Dawley rats within 48 h of 70% hepatectomy. Before LPS administration, plasma Fn or bovine serum albumin was given intravenously. RESULTS: The survival rate of the Fn-treated group was markedly improved compared with that of the controls. Fn prevented increases in the concentrations of serum enzymes and total bilirubin related to liver injury. The levels of inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1beta, and cytokine-induced neutrophil chemoattractant, in serum and liver tissue, also were significantly lower in the Fn-treated group than in the control group. Furthermore, the degree of apoptosis and necrosis in remnant liver was significantly decreased in the Fn-treated rats compared with the controls. CONCLUSIONS: These results indicate that Fn prevents endotoxin-induced liver injury after partial hepatectomy, at least in part through the inhibition of production of inflammatory cytokines, necrosis and apoptosis in the remaining liver.

Induction of inducible nitric oxide synthase in hepatocytes isolated from rats with ischemia-reperfusion injury.

BACKGROUND: Recent evidence indicates that nitric oxide (NO) has a crucial role in hepatic ischemia-reperfusion (I/R) injury. However, little is known about how I/R influences the gene expression of inducible nitric oxide synthase (iNOS) in hepatocytes. Under inflammatory conditions, we compared the induction of iNOS in hepatocytes isolated from normal and I/R-treated rats. METHODS: Hepatocytes were isolated using the collagenase perfusion method from rats treated with I/R (30-minute ischemia of middle and left lobes, followed by 3-hour reperfusion) or sham operation (control): Primary cultures of rat hepatocytes were incubated with an inflammatory cytokine, interleukin-1beta (IL-1beta), to compare the iNOS induction/NO production between the 2 groups. RESULTS: Both control and I/R groups had no production of nitrite (a stable metabolite of NO) in the absence of IL-1beta. In the control group, IL-1beta stimulated dose- and time-dependent production of NO. The I/R group showed more than 2-fold increased levels of NO production. Western and Northern blot analyses revealed that the I/R group also showed increased levels of iNOS protein and its messenger RNA. CONCLUSION: These results suggest that I/R directly affects the inducibility of the iNOS gene in hepatocytes by IL-1beta. Increased NO may be associated with protective or toxic effects in hepatic I/R injury.

Effects of pirfenidone on endotoxin-induced liver injury after partial hepatectomy in rats.

BACKGROUND: In living donor liver transplantation, restrictions on graft size are a serious obstacle to expand indications for adult recipients. The sequence of gram-negative infection, septicemia, and multiple-organ failure is a common cause of early mortality after liver transplantation. An effective therapy has not been established for endotoxemia following extended hepatectomy in donors or small-for-size grafts in recipients. Pirfenidone (PFD), a new experimental antifibrotic agent, was used to ameliorate on endotoxin-induced liver injury following partial hepatectomy. METHODS: Male Sprague-Dawley rats were intravenously administered lipopolysaccharide (LPS) 48 hours after 70% hepatectomy. Prior to LPS administration, PFD (300 mg/kg) or its vehicle (0.5% carboxymethylcellulose) was given orally twice. RESULTS: The survival rate of the PFD-treated group was markedly improved compared with that of the controls. PFD prevented the increases in the activities of serum enzymes (aspartate transaminase [AST], alanine transaminase [ALT], and lactate dehydrogenase [LDH]) and total bilirubin. The serum and liver tissue levels of inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1beta, interferon-gamma, and interleukin-6, were significantly lower among the PFD than the control group. Furthermore, the degree of necrosis in the remnant liver was significantly decreased in the PFD-treated rats compared with controls. CONCLUSION: These results indicate that PFD alleviates endotoxin-induced liver injury after partial hepatectomy through the inhibition of production of inflammatory cytokines in the residual liver. PFD may be useful to prevent endotoxin-induced liver injury after hepatectomy.

Effect of hepatocyte growth factor on induction of cytokine-induced neutrophil chemoattractant in rat hepatocytes.

BACKGROUND: Restrictions on graft size are a serious obstacle to the expansion of indications for adult recipients in living donor liver transplantation. Hepatocyte growth factor (HGF) has a crucial role in regeneration following hepatic injury. Rat cytokine-induced neutrophil chemoattractant (CINC), a member of the interleukin-8 superfamily in humans, has been implicated in chronic liver diseases or development of liver ischemia-reperfusion injury. Studies were performed to examine whether HGF influences the induction of CINC in hepatocytes. METHODS: Primary cultures of rat hepatocytes were treated with or without recombinant human (rh) HGF. The release of CINC into the culture medium and levels of CINC mRNA were measured using an enzyme-linked immunosorbent assay and Northern blot analysis. Transcription of nuclear factor (NF)-kappa B was detected by electrophoretic mobility shift assays. RESULTS: rhHGF increased the release of CINC in the medium dose- and time-dependently, showing a maximal effect at 100 ng/mL. Genistein (100 mumol/L) blocked the release of CINC stimulated by rhHGF. Levels of CINC mRNA were also increased, reaching a maximum at 8 hours after addition of rhHGF. Electrophoretic mobility shift assays revealed rhHGF activated transcription factor, NF-kappa B. CONCLUSION: These results suggest that HGF stimulates the induction of CINC gene expression through activation of NF-kappa B. CINC may be involved in the function of HGF during liver regeneration.

Pirfenidone protects endotoxin-induced liver injury after hepatic ischemia in rats.

BACKGROUND: Pirfenidone (PFD), an experimental antifibrotic agent, was investigated for its effects on endotoxin-induced liver injury after hepatic ischemia-reperfusion. METHODS: Male Sprague-Dawley rats were subjected to 30 minutes of partial hepatic ischemia, followed by reperfusion for 24 hours. Lipopolysaccharide (LPS) was injected at 30 minutes of reperfusion. PFD (300 mg/kg) or its vehicle (0.5% carboxymethylcellulose) was given orally following LPS administration. RESULTS: PFD prevented the increase in activities of serum alanine transaminase, aspartate transaminase, and lactate dehydrogenase after reperfusion. PFD inhibited the increase of cytokine-induced neutrophil chemoattractant in serum and liver tissue. The number of neutrophils infiltrating the liver was significantly lower in the PFD-treated group than the control group. CONCLUSION: These results indicate that PFD prevents endotoxin-induced liver injury after hepatic ischemia-reperfusion, in part through the decrease of neutrophil infiltration to the liver.

Effect of pirfenidone on induction of chemokines in rat hepatocytes.

BACKGROUND: Hepatic ischemia-reperfusion results in a neutrophil-dependent liver injury. The process of neutrophil recruitment and activation in this injury is at least partially dependent on the induction of chemokines, such as cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) in rats. In the liver, parenchymal cells (hepatocytes), in addition to nonparenchymal cells such as Kupffer cells, have been reported to produce chemokines in the regulation of hepatic inflammation. Pirfenidone (PFD) is a new experimental drug used as an antifibrotic agent. Studies were performed to determine whether PFD influences the production of CINC and MIP-2 stimulated by interleukin (IL)-1beta in a primary culture model of rat hepatocytes. METHODS: Primary cultures of rat hepatocytes were treated with IL-1beta in the presence and absence of PFD. The protein and mRNA of CINC and MIP-2 were analyzed using enzyme-linked immunosorbent assays and Northern blots. RESULTS: IL-1beta increased the release of CINC and MIP-2 into culture media in a dose- and time-dependent manner. PFD inhibited both CINC and MIP-2 release in dose-dependent fashion. However, PFD had no effect on the levels of CINC mRNA induced by IL-1beta. CONCLUSION: These results suggest that PFD inhibits the production of CINC and MIP-2 by IL-1beta at a posttranscriptional step in hepatocytes.

Fibronectin protects endotoxin-induced liver injury after partial hepatectomy in rats.

Endotoxemia following extended hepatectomy may be a cause of postoperative death. Multiple organ failure related to septemia is a common cause of early mortality after liver transplantation. Fibronectins (Fns) are involved in cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, and ischemic injury. Studies were performed to determine whether Fn influences the survival rate of rats subjected to endotoxin-induced liver injury after partial hepatectomy. Male Sprague-Dawley rats were intravenously administered lipopolysaccharide (LPS) 48 hours after 70% hepatectomy. Prior to LPS administration, plasma Fn or bovine serum albumin was given intravenously. The survival rate of the Fn-treated group was higher than that of the controls. Fn prevented increases in serum enzyme activity and total bilirubin related to liver injury. The levels of inflammatory cytokines including tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 interferon-gamma were also significantly lower in the Fn-treated than the control group. Furthermore, the number of apoptotic cells and the degree of necrosis in the remnant liver were significantly decreased in the Fn-treated rats compared with controls. These results indicate that Fn prevents endotoxin-induced liver injury after partial hepatectomy, at least in part through inhibiting the production of inflammatory cytokines, and the necrosis apoptosis in the remaining liver.

Safety of hepatectomy for living donors as evaluated using asialoscintigraphy.

In the living donor operation, accurate estimation of hepatic functional reserve is essential. Technetium-99m-galactosyl-human serum albumin (GSA) is a liver scintigraphy agent that binds to asialoglycoprotein receptors. We evaluated the preoperative assessment of the safety of an elective hepatectomy using GSA liver scintigraphy in 152 patients. GSA scintigraphy was performed after intravenous injection of GSA. The maximal removal rate of GSA (GSA-Rmax) was calculated using a radiopharmacokinetic model. We determined the areas for resection preoperatively depending on the operative procedures and calculated the local GSA-Rmax in the predicted residual liver (GSA-RL). A significant correlation was obtained between the GSA-Rmax and the 15-minute retention rate of indocyanine green. With sub- and monosegmentectomy, 2 patients had postoperative hepatic failure; in those 2 patients, the GSA-RL was 0.127 and 0.133, respectively, but these patients recovered well. Among those having di- and tri-segmentectomy, 5 patients experienced postoperative hepatic failure, in all subjects the GSA-RL was <0.15. Two patients died of postoperative liver failure 1 to 2 months after the operation. We concluded that GSA-RL is useful to select the procedure for hepatectomy in living donors and that GSA-RL should be >0.15 (mg/min/50 kg body weight) to avoid postoperative hepatic failure.

Functional hepatic regeneration following hepatectomy using galactosyl-human serum albumin liver scintigraphy.

In extended hepatectomy and liver transplantation, accurate estimation of functional hepatic regeneration is more important than volumetric regeneration. We investigated the usefulness of measuring the functional hepatic volume by 99m-technetium galactosyl-human serum albumin scintigraphy (GSA). Extended hepatectomy was performed in 32 patients. These patients were divided into subgroups with or without chronic hepatitis or cirrhosis. Functional hepatic volume GSA scintigraphy (GSA-LV) and determination of hepatic volume by CT (CT-LV) measurements were performed preoperatively, at 2 and 4 weeks and at 3 and 6 months after surgery. The preoperative GSA-LV values were significantly correlated with the hepatocyte volume and the 15-minute retention rate of indocyanine green (ICGR15). Similarly, the hepatocyte volume correlated well with the CT-LV and ICGR15. However, the CT-LV correlated only with the ICGR15. Recovery of the GSA-LV was delayed, and about 90% of the volumetric and functional regeneration was observed within 6 months after the hepatectomy. In contrast, the CT-LV in patients with normal liver remnants returned to approximately 90% of the initial volume within 1 month after the hepatectomy, whereas patients with injured livers regeneration showed gradual recovery to approximately 80% of the preoperative value by 6 months after hepatectomy. We conclude that measurement of functional hepatic volume using the GSA-LV is useful to evaluate hepatic function based on hepatocyte volume.

Fibronectin suppresses apoptosis and protects mice from endotoxic shock.

Multiple-organ failure related to septicemia is a common cause of early mortality after liver transplantation. Endotoxemia following living donor hepatectomy may be a cause of postoperative death. Plasma fibronectin (Fn) exerts a broad range of biological effects on cellular adhesion, motility, differentiation, apoptosis, hemostasis, wound healing, reticuloendothelial system function, and ischemic injury. We studied the therapeutic effect of plasma Fn in mice after an intraperitoneal injection of lipopolysaccharide (LPS) and d-galactosamine (GalN). Female Balb/c mice received simultaneous intraperitoneal injection of LPS (50 microg/kg) and GalN (400 mg/kg). Thirty minutes prior to GalN/LPS administration, plasma Fn or bovine serum albumin was given intravenously. A single administration of plasma Fn (500 mg/kg) protected in dose-dependent fashion against lethal shock after GalN/LPS challenge. Plasma Fn significantly reduced the serum tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 levels and significantly increased the serum interleukin-10 levels after GalN/LPS administration. Furthermore, plasma Fn significantly inhibited liver necrosis at 9 hours after GalN/LPS injection. The fraction of apoptotic-positive cells in these plasma Fn-treated mice was significantly lower than in the control group. These results support the protective treatment of endotoxin-induced liver injury by plasma Fn.

Clinicopathologic evaluation after resection for ductal adenocarcinoma of the pancreas: a retrospective, single-institution experience.

INTRODUCTION: Between April 1992 and December 2000, 167 patients with pancreatic carcinoma were evaluated and treated in our department. One hundred eight patients (64.7%) with pancreatic carcinoma underwent pancreatectomy. Of these patients, 94 had histologically proven ductal adenocarcinoma. The overall postoperative mortality rate was 3.2% (3 patients), and the morbidity rate was 35.1% (33 patients). The estimated 1-, 2-, 3-, and 5-year survival rates were 43.6%, 28.7%, 21.8%, and 12.9%, respectively. There were only six long-term survivors who survived >5 years after surgery. METHODOLOGY AND AIMS: Institutional experience with 94 consecutive patients with ductal adenocarcinoma who underwent pancreatectomy was reviewed to clarify the influence of 29 prognostic factors (5 host, 17 tumor, and 7 treatment factors). Special reference was made to determine whether these significant factors have an effect on long-term survival. Univariate and multivariate models were used to analyze the effect of prognostic factors on survival. RESULTS: Univariate analysis indicated that blood loss, operative time, postoperative complications, histopathologic lymphatic and venous permeation, lymph node metastasis, conclusive stage, conclusive curability, resection margins, serosal invasion, size of tumor, retroperitoneal invasion, major arterial invasion, and mode of histologic infiltration were associated with significantly longer survival (p < 0.05). By Cox proportional hazards survival analysis, the most powerful predictors of outcome were venous permeation, lymph node metastasis, tumor diameter, and conclusive curability. The longest-term survivor had the most advanced stage (stage IV(b)) of disease and curability C. No long-term survivors had all of the good prognostic factors (according to multivariate analysis). CONCLUSIONS: The prognosis after surgical resection of pancreatic carcinoma mostly depends on tumor factors. In this study, it was difficult to identify the determinants of long-term survival in patients with resectable tumors.