| Background: Helicobacter pylori(H.pylori)infection is the most important pathogenic factor,Stem cells are seed cells that regulate the self-renewal of the gastric mucosa and maintain its tissue integrity,which play an important role in the maintenance of gastric homeostasis and disease pathogenesis.It has been reported that gastric stem cells may undergo malignant transformation under the influence of carcinogenic factors.However,it is still not clear how H.pylori infection participates in the development of EGC by damaging gastric stem cells.Purpose: This study aims to explore the mechanism of action of H.pylori infection damaged gastric stem cells in the occurrence of early gastric cancer,and provide help for clinical diagnosis and treatment.Methods: Samples with pathological diagnosis of early gastric cancer that underwent Endoscopic submncosal dissection(ESD)in the digestive endoscopy center of our hospital were collected.The relevant clinical,pathological and endoscopic data were collected.The surface marker proteins of gastric stem cells were detected by immunohistochemistry and immunofluorescence staining.We further analyzed the clinical pathological features and the expression of the stem cell marker proteins.Results: A total of 142 patients with EGC were enrolled in this study,including 64 with current H.pylori infection,55 with previous H.pylori infection,and 23 without H.pylori infection.The clinical pathological data of 142 patients with early gastric cancer were analyzed.In terms of the atrophy range,60 cases(42.25%)had extensive atrophy.According to the histological gradeof tumor,103 cases were high grade,accounting for 72.54%.Compared with those without H.pylori infection,the adjusted odds ratio(OR)and 95% confidence interval(CI)of current H.pylori infection was 1.57(0.55-4.47)for extensive atrophy.The adjusted OR(95%CI)of current H.pylori infection was 1.07(0.34-3.39)for high grade.Immunofluorescence analysis showed that the expression intensity of six stem cell markers in H.pylori current infection was higher than that in non-infection.The fluorescence intensity of ASPM,AXIN2,LGR5,MIST1,TFF-2 and TROY in the current infection group was 39.54 ± 4.49,28.72 ± 6.78,31.98 ± 7.18,39.25 ± 7.31,38.90 ± 5.98 and 31.39 ± 6.40,respectively.The fluorescence intensity of the six stem cell markers in the non-infected group was 21.02± 2.04,22.17 ± 4.07,21.96 ± 4.75,21.30 ± 2.53,29.35 ± 4.98 and 15.38 ± 5.41,respectively.Immunohistochemical analysis only found that the comprehensive score of AXIN2 immunohistochemistry had statistical significance among groups with different H.pylori infection status.The comprehensive immunohistochemical scores of AXIN2 in H.pylori current infection,previous infection and non-infection were 3.90 ± 1.03,3.57 ±0.72 and 2.42 ± 1.46,respectively,P=0.002.In terms of thehistological grade of tumor,the immunofluorescence intensity of the high grade type and the low grade type TFF-2in H.pylori current infection was 40.79 ± 3.77 and 32.59 ± 7.95,P=0.0225;The immunofluorescence intensity of the high grade type and low grade type tumor type LGR5 in H.pylori previous infection was 29.49 ± 4.60 and 21.96 ± 4.51,P=0.0428.Conclusion: The results of the thesis suggest that H.pylori infection affects the clinical and pathological manifestations of early gastric cancer by upregulating stem cell markers such as AXIN2,LGR5,TROY,MIST1,TFF-2,and ASPM. |