| Gastric cancer is one of the most serious fatal tumors. It is listed the first position among various tumors in mortality. Study on the occurrence and developing mechanism of gastric cancer and explore reasonable and effective prevention methods will be very important for early prevention of gastric cancer and reducing the recurrence after operation.Epidemiology studies show that there is a significant relationship between Helicobacter pylori (Hp) infection and the development of gastric cancer. With infection of H. pylori the incidence of gastric cancer will increase 4-9 times. Hp has been listed the first class biologic carcinogenesis factor by WHO since 1994. As many other tumors, gastric cancer developing depends on not only a single factor but many factors. Those factors are involved in various stages of gastric cancer developing. It is now regarded that gastric cancer may be possible the results of the interaction between constant Hp infection and many other factors. Hp infection may be the first step factor. The comprehensive factors decide the final forming of gastric cancer. It has been reported these years that Hp cyto-toxin associated protein A ( CagA) positive strain had a stronger toxinability and been more dangerous. There is a close relationship between CagA+ strain and precancerous lesion and gastric cancer. Blaser et al studies showed that the CagA antigen positive H. pylori strain had increased the risk of gastric cancer. The prevalence rates of CagA+ Hp strain infection of different countries was compared by Perez - Perez. The rates ranged from 20. 6% to 82.2%. It was found that the infection rate had been much higher in developing countries than in developed ones. Webb et al compared the CagA+ Hp infection rates and gastric cancer mortalities of different countries, they said there had been a positive relationship between CagA + Hp infection and the mortality of gastric cancer. In order to discuss the possible etiologic association between CagA + Hp infection and gastric cancer associated diseases and gastric carcinogenesis, we have taken anepidemiological investigation on CagA + Hp strain infection status of high risk areas in Liaoning Zhuanghe, the high risk areas. See paperl.Cyclooxygense -2 (COX -2) is discovered by Dr. Simmons Lab before 10 years, COX - 2 possesses a similar function as COX - 1, they are isoenzymes. They are the rate - limiting enzyme in arachidonate metabolism. These enzymes catalyze the biosynthesis of prostaglandin H2, the precursor of molecules, such as prostaglandinE2, prostacyclin, and thromboxanes. COX -2 is an inducible enzyme that is normally absent from cells, but whose expression is rapidly and transiently induced by various stimuli, such as mitogens, cytokines and tumor promoters, it is involved in many inflammatory reactions. In contrast, COX - 1 is constitutively expressed in many tissues, it is involved in the homeostasis of various physiologic functions. Aspirin and other nonsteroidal anti - inflammatory drugs ( NSAIDs) inhibit both COX -1 and COX -2.Recent studies show that COX - 2 is over expressed in colorectal cancers,esophageal carcinoma etc. COX - 2 is induced in animal model familial adenom-atous polyposis. Accumulating evidence indicates that NSAIDs can reduce the incidence of colorectal cancers in human and experimental animals and can reduce the number and size of polyps in patients with familial adenomatous polyposis ( FAP) , NSAIDs and COX - 2 inhibitors can induce apoptosis of tumor cells. Accumulating evidences indicate that COX - 2 plays an important role in carcinogenesis. Hp infection is an inflammatory reaction, whether COX -2 is induced by it? Whether other cytokines are induced by it ?Romano et al studies show that Hp did not affect COX - 1 expression, whereas COX - 2 mRNA levels increased by 5 - fold at 24h after incubation of MKN 28 cells with broth culture filtrates or bacterial suspensions from wild -type Hp strain. Also Hp caused a 3 - fold increase in the release of prostaglandin E2, the main product of cy...
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