| Malignant tumor is one of the major disease considerablythreatening to human health, and its wide spread invasion and metastases to vitalorgan are the leading causes of mortality.H.pylori infection is a significant pathogenic mechanism and independentdangerous factor for precancerous lesions such as peptic ulcer or gastriccarcinoma, thus, the working group of International Agency for Research onCancer (IARC) of World Health Organization have already classified it as aclass I carcinogen.H.Pylori is a microaerophilic, Gram-negative, spiral bacterium. SinceAustralian researchers Warren and Marshall successfully isolated H.pylori ingastric mucosa from a patient with gastritis for the first time in 1983, studies onH.Pylori have become a hot spot in research fields.A great number of researcheshave shown the close relationship between H. pylori and the occurrence ofdiseases in gastro intestinal tract (GIT) like dyspepsia, chronic gastritis, peptic ulcer, MALT lymphoma and gastric cancer. H.Pylori is a chief risk factor ofchronic gastritis and peptic ulcer, and also one of the causative factors of gastricadenocarcinoma as well as gastric lymphoma. There is an extremely highinfection rate of H, pylori around the world with 30% to 50% of adults in thedeveloped countries and 40% to 80% in the developing countries.Epidemiological studies in China showed a high result of 40% to 90% and anaverage rate of 59%. Therefore, the infection of H. Pylori has been drawingmore and more attention among People.Objective: To investigate the possible role of Helicobacter pylori (Hp)infection in the development of gastric cancer.Method: Hp was assessed by using rapid urease staining test.Immunohistochemical staining was used to detect the expression of CDK1 in 30Cases of chronic superficial gastritis (CSG), 30 cases of chronic atrophicgastritis (CAG) and 30 cases of gastric cancer (GC) (HP-positive group in 15cases, 15 cases of negative in each group).Results:The positive expression rates of CDK1 (47%) and CDK1 (76%) inchronic atrophic gastritis and gastric cancer were significantly higher thanchronic superficial gastritis((16.6%) (P<0.05). There was no significantdifference in the positive rate of CDK1 between Chronic Superficial Gastritiswith HP positive patients and Hp negative patients (P>0.05). In CAG, GC,CDK1 protein expression level was increased in H. pylori positive patients whencompared with H. pylori negative patients (P<0.05). Conclusion: CDK1 gene expression is accelerated in gastric cancer andchronic atrophic gastritis. HP might act as a tumor promoter in the genesis ofgastric carcinoma. |