胃癌与端粒酶及幽门螺杆菌感染的相关关系

目的探讨幽门螺杆菌(Hp)感染对胃黏膜端粒酶活性的影响及与胃癌的相关性.方法用端粒酶重复序列扩增法(TRAP)检测66例胃癌、30例萎缩性胃炎及20例正常胃黏膜标本端粒酶活性,以尿素酶法及病理组织学方法检测Hp感染.结果端粒酶活性检出率及Hp感染率分别为:正常胃黏膜10%(2/20)、35%(7/20);萎缩性胃炎36.6%(11/30)、43.3%(13/30);胃癌89.5%(59/66)、66.6%(44/66).被检标本的二者检出率随病变加重而增高.Hp感染标本的端粒酶活性检出率比无Hp感染者高.三组资料χ2检验优势比,胃癌组OR值=6,提示Hp阳性者的危险性是Hp阴性者的6倍,有显著性差异.但不论有无Hp感染,其端粒酶检出率均随病变程度加重而增加.正常胃黏膜标本中有端粒酶活性检出的标本均有Hp感染,而从胃炎及胃癌标本中检出的端粒酶阳性标本有60%以上有Hp感染.结论端粒酶活性检测可作为胃癌诊断的参考指标;Hp感染可激活端粒酶,加速胃黏膜损伤,引起一系列的病理改变可能与胃癌发生有关.

The effect of helicobacter pylori Infection on telomerase expression and gastric carcinogenesis

Objective To analyse the correlation between the Hp infection and telomerase activaty with gastric mucosa pathology.Methods Telomerase activity was evaluated by the telomerase repeat amplification protocol assay (TRAP).Helicobacter pylori (Hp) infection was identified by urease assay and pathomorphology.Results Telomerase activity and Hp infection were detected in 2 of 20 (10%) and 7 of 20 (35%) normal gastric mucosa,11 of 30 (36.6%) and 13 of 30 (43.3%) atrophic gastritis,59 of 66 (89.5%) and 44 of 66 (66.6%) primary gastric cancer respectively.Both detection rates in assessed specimens increased with the pathological changes from normal to cancer.The detection rate of telomerase in Hp infected specimens was higher than that in the uninfected. However,it increased with stage of pathological changes no matter the specimen was infected or not.All telomerase-positive specimens were from normal gastric mucosa,while the majority(>60%) of those from atropic gastritis and cancer was in fected with Hp.Conclusions These findings suggest that telomerase activity may be a useful marker for evaluating gastric cancer.Hp infection can activate telomerase,which accelerates the injury of gastric mucosa and the result in a series of pathological changes and carcinogenesis.