Background:This multicentre randomised phase III trial was designed to determine whether adjuvant chemotherapy with gemcitabine improves the outcomes of patients with resected pancreatic cancer.Methods:Eligibility criteria included macroscopically curative resection of invasive ductal carcinoma of the pancreas and no earlier radiation or chemotherapy. Patients were randomly assigned at a 1 : 1 ratio to either the gemcitabine group or the surgery-only group. Patients assigned to the gemcitabine group received gemcitabine at a dose of 1000 mg m−2 over 30 min on days 1, 8 and 15, every 4 weeks for 3 cycles.Results:Between April 2002 and March 2005, 119 patients were enrolled in this study. Among them, 118 were eligible and analysable (58 in the gemcitabine group and 60 in the surgery-only group). Both groups were well balanced in terms of baseline characteristics. Although heamatological toxicity was frequently observed in the gemcitabine group, most toxicities were transient, and grade 3 or 4 non-heamatological toxicity was rare. Patients in the gemcitabine group showed significantly longer disease-free survival (DFS) than those in the surgery-only group (median DFS, 11.4versus 5.0 months; hazard ratio=0.60 (95% confidence interval (CI): 0.40–0.89); P=0.01), although overall survival did not differ significantly between the gemcitabine and surgery-only groups (median overall survival, 22.3 versus 18.4 months; hazard ratio=0.77 (95% CI: 0.51–1.14); P=0.19).Conclusion:The current results suggest that adjuvant gemcitabine contributes to prolonged DFS in patients undergoing macroscopically curative resection of pancreatic cancer.

The aggravated coagulation parameters predict a fatal outcome in patients with acute pancreatitis. AT-III level (<69%) was the most accurate marker for poor outcome of acute pancreatitis at admission.

PSE can reduce the platelet pool and induce an increase in platelet count. This increase is greatly dependent on the infarcted splenic volume.

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In previous studies, the gene expression profiles of two hamster pancreatic cancer cells with different potentials for invasion and metastasis were analyzed. In the present study, we identified that one of the genes expressed strongly in the highly metastatic cell line is hamster oxysterol binding protein-related protein (ORP)-5. The aim of the present study was to clarify the relationship between ORP5 and invasion and poor prognosis of human pancreatic cancer. Invasion assays were carried out in both hamster and human pancreatic cancer cells by suppressing the ORP5 gene with short interfering RNA or inducing its expression by introducing an expression vector. To evaluate the relationship between ORP5 and the characteristics of human pancreatic cancer, 56 pancreatic cancer tissue specimens were analyzed and the ORP5 expression in each pancreatic cancer tissue specimen was analyzed by immunohistochemistry. In both the hamster and human pancreatic cancer cells, suppression of ORP5 significantly reduced the invasion rate of the cells and induction of ORP5 significantly enhanced the invasion rate of the cells. In the clinical sample, the median survival times of the patients with ORP5-positive (n = 33) and ORP5-negative (n = 23) cancer were 8.3 and 17.2 months, respectively (P = 0.02). Also, the 1-year survival rates of patients with ORP5-positive and ORP5-negative cancer were 36.4 and 73.9%, respectively (P = 0.005). The ORP5 expression level was related to both invasion and poor prognosis in human pancreatic cancer. These findings suggest that the expression of ORP5 may induce cancer cell invasion, resulting in the poor prognosis of pancreatic cancer. (Cancer Sci 2008; 99: 2387-2394) P ancreatic cancer is one of the most malignant tumors. In most cases, patients are already at an advanced stage of the disease at the time of diagnosis. The main reason for the poor prognosis is not only that these cancers are difficult to detect by ultrasonography or computed tomography, but also that they exhibit great potential for invasion and metastasis. To establish an effective treatment strategy for pancreatic cancer, it is necessary to clarify the cellular and molecular mechanisms of invasion and metastasis in pancreatic cancer.In our previous studies, we established two hamster pancreatic cancer cell lines with different potentials for invasion and metastasis: PC1, possessing a low potential for invasion and metastasis, and PC1.0, possessing a high potential for invasion and metastasis. These two cell lines were established from the same pancreatic ductal carcinoma induced by N-nitrosobis (2-oxopropyl) amine in a Syrian golden hamster.(1,2) Moreover, PC1.0 cell lines were found to produce a soluble proteinaceous factor in the medium; this factor was found to induce cell dissociation and therefore we designated it the 'dissociation factor'. (3)(4)(5) We hypothesized that isolation of this factor might provide great insight into the molecular and cellular mechanisms of pancreatic cancer invasion and metastasis, and we therefo...