Abstract

G A A b st ra ct s pancreatic cancer, as well as acute and chronic pancreatitis. Methods: Orthotopic pancreatic cancer model was created by surgical injection of 500,000 S2VP10 cells. Once palpable tumors were established, blood samples were collected. Acute pancreatitis models were created by serial injections of supramaximal concentration of cerulein (50μg/kg) at hourly intervals for a total of ten hours. One hour after the last injection, the mice were sacrificed and bled by cardiac puncture. Chronic pancreatitis was induced by biweekly injections of high dose cerulein (50 μg/kg x6) for 10 weeks, followed by animal sacrifice and bleeding by cardiac puncture. All serum samples were analyzed by sandwich ELISA using a capture antibody specific for the inducible form of HSP-70. The ELISA results were then confirmed by serum immunoprecipitation followed by Western blotting to comparatively assess the serum HSP-70 levels. Results Five mice in each category of acute pancreatitis, chronic pancreatitis, and orthotopic cancer models were used to determine serum HSP-70 levels. No inducible HSP-70 was detected in the control group. The serum HSP-70 levels for all models were significantly higher than controls with all P-values of 0.3. Conclusions Serum HSP-70 is elevated inmicewith orthotopic pancreatic cancer, acute pancreatitis and chronic pancreatitis, without significant difference between the groups. Further research will focus on its role as a prognostic marker in pancreatitis and pancreatic cancer.

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