Association Between Serum Pepsinogen And Expression Of COX-2 In Gastric Cancer And Precancerous Lesion

Cancer of the stomach is one of the most frequent and lethal malignancies in the world. Etiopathogenesis of gastric cancer is complex and incompletely understood.Record linkage studies have found the relationship between the serum PG levels and the expresstion of Cyclooxygenase and gastric malignancy.Pepsinogens(PG) produced by chief human gastric mucosa are classified into two immunologically distinct groups. pepsinogen I(PG I),which is derived from chief and mucus neck cells,and pepsinogen II (PG II),which is derived from cardiac glands,pyloric glands and Brunners glands.As well as chief and mucus neck cells The two pepsinogens not only are secreted into the lumen of the gastrointestinal tract.but also enter the blood circulation.It is believed that the blood pepsinogen level reflects the morphological and functional status of the gastric mucosa.Many recent foreign and domestic reports showed the human serum pepsinogen(PG) levels were valuable in the diagnosis of gastric Diseases .the serum PGI and PGR levels in patients with gastric cancer and the atrophic gastritis are much lower.But the mechanism of the decrease of the serum PG levels. Cyclooxygenase (Cox) is the key enzyme in conversion of arachidonic acid to prostanoids. Two Cox genes have been cloned (Cox-1 and Cox-2) that share over 60% identity at amino acid level and have similar enzymatic activities .The most striking difference between the Cox genes is in the regulation of their expression. Whereas Cox-1 is constitutively expressed, and the expression is not usually regulated, expression of Cox-2 is lowor undetectable in most tissues but can be highly induced in response to cell activation by hormones, proinflammatory cytokines, growth factors, and tumor promoters. COX-2 is an inducible immediate-early gene,and its role has been connected to inflammation,reproduction, and Carcinogenesis.a number of researches show that COX-2 was expressed at a very high level in gastrointestinal tumors.Record linkage studies also have found a lower incidence of gastrointestinal cancers among patients with rheumatoid arthritis .Because these patients use extensive amounts of NSAIDs,The best known target of NSAIDs is COX.However, we know less about the relationship between COX-2 Overexpression and the serum PG levels from chronic superficial gastritis,atrophic gastritis to gastric cancer group.Objective: To explore Correlation between Serum Pepsinogen and expression of COX-2 in gastric cancer and precancerous lesion。Method: These patients were divided into 3 groups based on endoscopic and histopathological findings: 29 patients in chronic superficial gastritis,57 patients in atrophic gastritis group, 36 patients in gastric cancer group, Fasting serum samples for PGⅠand PGⅡ, determination were analyzed by Latex-enhanced。Immunohistochemical staining was used to detect the expression of COX-2。Results: From chronic superficial gastritis group,atrophic gastritis group to gastric cancer group,the PGⅠand PGR values gradually decreased and the expression rate of COX-2 gradually increased (P<0.05)。the PGⅠand PGR values decreased significantly in COX-2 positive of atrophic gastritis group AND gastric cancer group when compared with COX-2 negative patients. the PGⅠdecreased significantly in COX-2 positive patients of atrophic gastritis group AND gastric cancer group when compared with COX-2 positive patients of chronic superficial gastritis. But the PGⅠdid not decrease significantly in COX-2 positive patients of gastric cancer group when compared with COX-2 positive patients of atrophic gastritis group Conlusions: the expression of COX-2 in gastric cancer and precancerous lesion can influence the serum PG levels.the gastric mucosa expression of COX-2 can make the serum PGI level lower. But this influnce is more obviously from chronic superficial gastritis group to atrophic gastritis group .From atrophic gastritis group to gastric cancer group this influnce not obviously.COX-2 might act as a tumor promoter in the genesis of gastric carcinoma.