| Background: Gastric carcinogenesis is a process of many etiological factors and steps, and concerns with the abnormal alterations of many kinds of oncogenes, tumor suppressor genes, the scenario of these changes result in the gastric cancer. Now, Helicobacter pylori (Kpylori) is correlative with the gastric cancer, the International Agency for Research on Cancer has termed H.pylori as group I carcinogen, a definite cause of cancer in humans, but the precise mechanism remains unclear. It has been reported that telomerase activity can be detected in many human tumor cells, as a consequence, the activation of telomerase might be a key step of carcinogenesis. The oncogene and tumor suppressor gene such as c-myc and p16 maybe have some roles during stomach cancer progression. The purpose of this research was to explore the mechanism of the gastric carcinogenesis by studying the relation between H.pylori infection and telomerase activity and the expression of c-myc , p16 in the process of gastric tumor genesis.Objective:1. To study the action of telomerase activity in the process of gastric tumor genesis and the relationship between telomerase activity and clinicopathological factors such as sex, tumor location, size gross type and microsxopic morphology.2. To elucidate the relationship between H.pylori and telomeraseactivity by detecting the Hpylori infection and telomerase activity in the gastric mucosa.3. To explore the mechanism of H.pylori resulting in the gastric cancer and to reveal the stomach cancinogenesis by detecting the expression of c-myc, p16 and H.pylori infection and telomerase activity in gastric mucosa.Methods:l.171gastric biopsy specimens were obtained from upper gastrointestinal endoscopy or surgery operation. All subjects were diagnosed with histopathology: 20 chronic superficial gastritis (CSG), 30 chronic atrophic gastritis (CAG) with mild degree intestinal metaplasia(IM), 42 chronic atrophic gastritis with moderate, severe degree intestinal metaplasia, 14 dysplasia(Dys), 65 gastric cancer(GC). H.pylori was detected by rapid urea enzyme test and bacteria culture. We considered for the H.pylori infection if they are all positive.2. Serum H.pylori-CagA-IgG was determined by enzyme immunoassay in the patients with H.pylori positive and CAG with moderate, severe IM. CagA+Hp and CagAHp team was determined according the CagA protein.3. Telomerase activity of gastric biopsy specimens was detected by PCR-ELISA.4.The expression of c-myc and p16 were studied by immunhistochemical technique.Results:1 .Detection of H.pylori and telomerase activity 112 of 171 subjects were H.pylori (+). The Rpylori infection in CSG was 65%( 13/20); CAG with mild degree IM was 60%(18/30); CAG withmoderate, severe degree IM was 66.67%28/42); Dys was 64.29%(9/14); GC was 67.69%(44/65). Hpylori infection had no significant difference among these groups.The positive rates of telomerase activity of all samples varied as follows: CSG was 0; CAG with mild degree IM was 13.33%(4/30); CAG with moderate , severe degree IM was 52.38%(22/42); Dys was 35.71%(5/14); GC was 87.69%(57/65). The telomerase activity in gastric cancer ranked the highest (p<0.01); the telomerase activity in CAG with moderates severe degree IM was significantly higher than CAG with mild degree IM (P<0.05).2.Relationship between telomerase activity and clinicopathological factors in gastric cancer29 gastric cancers with complete clinical data was grouped by sex, tumor location, size gross type and microscopic morphology, the telomerase activity among these groups has no significant difference (P>0.05)3.Expression of c-myc and p16 in gastric mucosa The expression of c-myc were 5%(1/20), 16.67%(5/30), 47.62%(20/42), 57.14%(8/14), 61.54%(40/65) in CSG, CAG with mild degree IM, CAG with moderate, severe degree IM, GC respectively. The expression of c-myc in gastric cancer ranked highest. The expression of c-myc in CAG with moderate, severe degree IM was significantly higher than CAG with mild degre... |
