Background-Helicobacter pylori species comprise diVerent strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern. Aims-(1) To evaluate the polymorphism of the vacA gene and to ascertain whether the cagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting. Patients-Twenty one patients with gastric adenocarcinoma and 71 with H pylori associated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis). Methods-The polymerase chain reaction was used to verify the presence or absence of cagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against diVerent H pylori antigens by western blotting. Results-cagA gene and the allele s1 of vacA were significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) ( 2 =16.01, p<0.001; and 2 =13.97, p<0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases. Conclusions-H pylori infection caused bycagA positive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pylori antigen in patients with gastric adenocarcinoma is important.

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In this study we assessed whether conditioned media from a human pancreatic cancer cell line (MIA PaCa 2) can interfere with some intracellular pathways involved in glucose metabolism in isolated rat hepatocytes. The hepatocytes. isolated from Male Wistar rats, were incubated with MIA PaCa 2-conditioned or nonconditioned media. Conditioned and nonconditioned hepatocytes were run for 120 min in the presence or absence of insulin (100 m M ) and were sampled at fixed time intervals. Supernatant glucose levels decreased to a similar extent over time in both conditioned and nonconditioned hepatocytes, while lactate levels significantlly increased in nonconditioned hepatocytes with respect to conditioned hepatocytes. A pyruvate kinase activity increase was observed only in nonconditioned hepatocytcs and was biphasic in nature, since this increased activity was dctccted both after a few and after 30 min following insulin stimulation. The cyclic A M P level increase was significantly higher in conditioned than in nonconditioned hepatocytes. It appears that MIA PaCa 2 cells produce a factor(s) that may interfere with one of the insulin-mediated intracellular pathways of glucose metabolism, namely, glycolysis. This detrimental effect on glycolysis is supported by the blunted rise in lactate concentration in the medium after the glucose challenge. This substance(s) probably transfers its signal inside the target cells, activating the adenylate cyclase pathway. These results support the hypothesis that pancreatic cancer is the cause rather than the consequence of diabetes mellitus. Key Words: Pancreatic cancer-Diabetes mellitus-MIA PaCa 2.Severall literature studies demonstrate a link between paincreatic cancer and altered glucose homeostasis (1-11). Overt diabetes mellitus and/or a reduced glucose tolerance are found in -80% of patients with pancreatic cancer (2,5,7). Several in vivo and in viiro studies attempted to identify the pathophysiological mechanism(s) responsible for the association between pancreatic cancer and diabetes mellitus. It hlas been shown that pancreatic cancerassociated diabetes does not depend on the destruction of pancreatic p cells (5,7,9) but, rather, on the Manuscript Address corrcspondence and reprint requcsts to Dott. M. Plebani.