胃癌与肠化生关系密切。
Gastric carcinoma closely relates with intestinal metaplasia.
胃的肠化生在幽门螺杆菌高感染率的国家普遍存在。
Gastric intestinal metaplasia is a common finding in countries with a high prevalence of Helicobacter pylori infection.
非典型增生显然是肿瘤发生的最大危险因素，超过了肠化生。
Dysplasia clearly represents the greatest risk for subsequent development of cancer, certainly more than gastric intestinal metaplasia.
然而癌前病变是已经公认的肠化生还是更难于探及的不典型增生。
Yet is the premalignant lesion the readily recognized intestinal metaplasia or the more difficult to detect dysplasia?
公认的肠化生或更难发现的异型增生是否做为癌前病变得到检测？
Is the premalignant lesion to be detected the readily recognized intestinal metaplasia or the more difficult to detect dysplasia?
P 27在胃癌、异型增生、肠化生组织中的表达较正常胃黏膜降低。
The expressions of P27 in gastric hyperplasia, intestinal metaplasia and gastric carcinoma tissues were lower than that in normal gastric mucosa.
目的：了解幽门螺杆菌（HP）感染伴胃黏膜肠化生者经根除HP后肠化生的变化情况。
Objective:To observe the effect of Helicobacter pylori (HP) eradication on intestinal transdifferentiation in chronic gastritis.
此外，几项回顾性研究表明食管柱状上皮肠化生能很好的界定腺癌的发病风险，而杯状细胞不能。
In addition, several retrospective and outcome studies suggest a well-defined risk of neoplasia in patients with esophageal columnar metaplasia, but without goblet cells.
肠化生硫酸粘液阴性、阳性两组与不同程度不典型增生各组pcna、P 53、CEA表达情况比较稍有不同。
Expressions of PCNA, P53, CEA are a little difference between various dysplasias and intestinal metaplasia with Sulphuric acid mucus or without Sulphuric acid mucus.
结论：p 53蛋白可在胃癌的早期诊断中起作用，其改变在胃癌发生的早期即居于肠化生阶段的癌前变化过程中。
Conclusion: P53 protein can be used in early clinical diagnosis. Early in gastric carcinogenesis, its change occurs at intestinal metaplasia stage.
结论肠化生组织中MSI的进行性积累可能在一部分胃癌的发生中起作用，MSI可能是胃癌发生的早期分子事件。
Conclusion The progressive accumulation of MSI in areas of IM may contribute to gastric carcinogenesis and MSI may be an early and imoprtant molecular event in gastric carcinogenesis.
提示HP感染是肠上皮化生的促进因素之一，继而增加患胃癌的危险性。
It indicated that HP infection may be one of the factors to induce intestinal metaplasia and so to increase the risk of carcinoma of stomach.
目的：探讨CDX2和PTEN蛋白表达与胃黏膜肠上皮化生的关系。
Objective: To study the relationship of expression of CDX2 and PTEN proteins and gastric metaplasia .
胃癌中部分患者并不经历肠上皮化生或异型增生阶段。
Some gastric cancer patients did not undergo intestinal metaplasia or gastric mucosa dysplasia.
结论对胃黏膜异型增生和肠上皮化生等病变患者的胃镜随访有利于提高胃癌(特别是早期胃癌)的检出率。
Conclusion Gastroscopy and follow-up of patients with intestinal metaplasia or gastric mucosa dysplasia help to detect gastric carcinoma, especially early-stage gastric carcinoma.
作者认为，除注意肠上皮化生和萎缩性胃炎等表现外，各种不典型增生现象也很重要。
Beyond the well known intestinal metaplasia and chronic gastritis, we found also other atypia or dysplasia.
多种因素与胃癌的发生相关，如环境、饮食、幽门螺杆菌感染、慢性萎缩性胃炎和肠上皮化生等。
There are well-known risk factors for gastric cancer such as environment, foods, Helicobacter pylori infection of the stomach, chronic atrophic gastritis and intestinal metaplasia.
结果：由慢性浅表性胃炎→胃粘膜肠上皮化生→轻度异型增生→重度异型增生→胃癌，端粒酶阳性率逐渐增高，分别为0 %、42 9%、40 0 %、75 0 %、84 0 %。
Results: The positive rate of telomerase in chronic superficial gastritis, intestinal metaplasia, mild dysplasia, severe dysplasia and gastric cancer was 0%, 42.9%, 40.0% 75.0%, 84.5% respectively.
结果：由慢性浅表性胃炎→胃粘膜肠上皮化生→轻度异型增生→重度异型增生→胃癌，端粒酶阳性率逐渐增高，分别为0 %、42 9%、40 0 %、75 0 %、84 0 %。
Results: The positive rate of telomerase in chronic superficial gastritis, intestinal metaplasia, mild dysplasia, severe dysplasia and gastric cancer was 0%, 42.9%, 40.0% 75.0%, 84.5% respectively.
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