Cap43 has been identified as a nickel-and calcium-induced gene, and is also known as N-myc downstream-regulated gene 1 (NDRG1), Drg-1 and rit42. It is also reported that overexpression of Cap43 suppresses metastasis of some malignancies, but its precise role remains unclear. In this study, we asked how Cap43 could modulate the tumor growth of pancreatic cancer. Stable Cap43 cDNA transfectants of pancreatic cancer cells with Cap43 overexpression showed similar growth rates in culture as their control counterparts with low Cap43 protein level. By contrast, Cap43 overexpression showed a marked decrease in tumor growth rates in vivo. Moreover, a marked reduction in tumor-induced angiogenesis was observed. Gelatinolytic activity by matrix metalloproteinase-9 and invasive ability in Matrigel invasion activity were markedly decreased in pancreatic cancer cell lines with high Cap43 expression. Cellular expression of matrix metalloproteinase-9 and two major angiogenic factors, vascular endothelial growth factor and interleukin-8, were also significantly decreased in cell lines with Cap43 overexpression as compared with their parental counterparts. Immunohistochemical analysis of specimens from 65 patients with pancreatic ductal adenocarcinoma showed a significant association between Cap43 expression and tumor microvascular density (P = 0.0001) as well as depth of invasion (P = 0.0003), histopathologic grading (P = 0.0244), and overall survival rates for patients with pancreatic cancer (P = 0.0062). Thus, Cap43 could play a key role in the angiogenic on-or offswitch of tumor stroma in pancreatic ductal adenocarcinoma.

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This report describes a 49-year-old woman with recurrent massive gastrointestinal bleeding from jejunal varices without portal hypertension. Preoperative diagnosis was obtained by abdominal computed tomography, superior mesenteric arterial angiography and percutaneous transhepatic portography. Percutaneous transhepatic portographic findings revealed no step-up of oxygen concentration and normal pressure in the portal vein, only dilation of superior mesenteric vein. Jejunal resection and anastomosis resulted in complete resolution of the bleeding, and the patient has experienced no recurrent bleeding over a 4 year follow-up period. A review of the literature shows that this syndrome is nearly always characterized by portal hypertension, generally due to liver cirrhosis. Accurate preoperative diagnosis is often difficult. We report a very rare case of jejunal varices without portal hypertension.

Depletion of sarcolemmal membrane dystrophin occurred during cardioplegic arrest and reperfusion. Nicorandil preconditioning may attenuate ischemia and reperfusion injury by maintaining the membrane structural integrity.

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