| Pancreatic carcinoma is a highly malignant tumor of digestive tract. Its incidence has been increasing steadily in recent 40 years. The 5-year survival rate is only 1-4%, with a nearly equalized incidence and mortality. Up to now, there has been no effective clinical therapeutic method in treating this malignancy.For a number of solid tumors, including pancreatic cancer, efforts aimed at disease prevention may be more successful than currently available anti-cancer treatment. Therefore, it is very important to search for an effective chemical preventive method to decrease the incidence and mortality of pancreatic carcinoma.Chemical prevention is the utilization of pharmacological or natural agents to prevent, suppress, interrupt or reverse the process of carcinogenesis. Beside anti-inflammatory, anti-febrile, analgesic and inhibitory effects on blood platelet aggregation, non-steroid anti-inflammatory drugs (NSAIDs) process inhibitory effects on tumor cell proliferation and is able to induce tumor cell apoptosis. The chemical prevention properties of these agents on GI tumors have been confirmed by many studies, but their role in pancreatic carcinoma prevention and treatment is poorly understood, and the results are contradictory. Curcumin, isolated from turmeric (Curcuma) having some characteristics of NSAIDs, has significant anti-oxidation, anti-mutation and anti-carcinoma effects. At present, most attentions are focused on chemical prevention of tumors. Although it has been listed the 3rd generation of chemical preventive agents for carcinoma in USA, reports about its direct anti-carcinoma are rare.In this article, we compared in vitro inhibition effects of Curcumin, selective and non–selective NSAIDs on pancreatic carcinoma in order to see if there is synergistic effort of Curcumin combing with NSAIDs; and therefore decreasing the dosage of NSAIDs and reducing its side-effect; and the molecular mechanisms of anti-carcinoma of Curcumin and NSAIDs were also discussed.Chapter One: Expression and Significance of COX-2 and Survivin in Pancreatic Carcinoma Tissues1. Objectives: To discuss the expression of COX-2 and Survivin in human pancreatic carcinoma tissues and their relationships with pancreatic carcinoma.2. Methods: Tissue specimens in 48 cases of pancreatic carcinoma, 10 cases of chronic pancreatitis, 5 cases of normal pancreas were embedded paraffin All of the patients did not undergo chemotherapy or radiotherapy before operation. Immuno-histochemistry with En vision 2 steps method was employed using rabbit serum and 0.01M PBS as the 1st antibody respectively to determine its specificity and reliability. According to stain intensity in cytoplasm or nucleolus and the ratio of staining cell, negative, weak positive, positive and strong positive was used to express the results. SPSS 10.0 software was used to perform variance and statistical significance exists if p<0.05.3. Results: COX-2 expression in pancreatic carcinoma tissues (88.3%) was markedly higher than that in chronic pancreatitis, and there was no COX-2 expression in normal pancreatic tissues. There was significant difference between pancreatic carcinoma and chronic pancreatitis (Z=-3.647, P=0.0001<0.01), and between pancreatic carcinoma and normal pancreatic tissues (Z=-3.217, P=0.01).But no significant difference between chronic pancreatitis and normal pancreatic tissues(Z=-1.316, P=0.188>0.05). Survivin was only expressed in pancreatic carcinoma, the positive rate was 56.25%, but it was not found in chronic pancreatitis and normal pancreatic tissues. There was significant difference between pancreatic carcinoma and normal pancreatic tissue (Z=-2.215, P=0.027<0.059) There was significant difference between pancreatic carcinoma and chronic pancreatitis tissues (Z=-3.050, P=0.02<0.05); There was no significant difference between well differentiated and poorly differentiated carcinoma cells (Z=-1.237, P=0.216>0.05); COX-2 and Survivin were coexisted. There was no significant difference between COX-2 and Survivin expressions(X2=2.
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