Gastric carcinoma closely relates with intestinal metaplasia.
胃癌与肠化生关系密切。
Chronic gastritis with intestinal metaplasia, negative for dysplasia or malignancy.
慢性胃炎伴肠化，无异型增生或恶性肿瘤。
Usually it arises in a background of chronic atrophic gastritis with intestinal metaplasia.
背景通常为慢性萎缩性胃炎伴肠化。
Some gastric cancer patients did not undergo intestinal metaplasia or gastric mucosa dysplasia.
胃癌中部分患者并不经历肠上皮化生或异型增生阶段。
Beyond the well known intestinal metaplasia and chronic gastritis, we found also other atypia or dysplasia.
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。
Yet is the premalignant lesion the readily recognized intestinal metaplasia or the more difficult to detect dysplasia?
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。
Gastric intestinal metaplasia is a common finding in countries with a high prevalence of Helicobacter pylori infection.
胃的肠化生在幽门螺杆菌高感染率的国家普遍存在。
Liver cell is the metabolic one of intestinal metaplasia, it functions to transport and digest, should belong to spleen.
肝细胞是肠上皮特化的代谢细胞，其功能主运化，当归属脾藏。
The problem is the low prevalence of the premalignant lesion being assessed (ie, dysplasia in gastric intestinal metaplasia).
该问题是评估低流行癌前病变(如，胃肠化生中的非典型增生)。
Is the premalignant lesion to be detected 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？
TLR4 expression in gastric mucosa with intestinal metaplasia, dysplasia is significantly higher than that in gastric cancer mucosa.
肠化、不典型增生胃粘膜组织tlr4的阳性表达明显高于胃癌组织。
Dysplasia clearly represents the greatest risk for subsequent development of cancer, certainly more than gastric intestinal metaplasia.
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。
At the same time, RNA dot blot revealed that the expression of hTR was increased with intensified intestinal metaplasia in gastric mucosa.
同时RNA斑点杂交结果提示在非癌胃组织中随着肠化程度增高人端粒酶rna表达也增强。
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.
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。
The expressions of P27 in gastric hyperplasia, intestinal metaplasia and gastric carcinoma tissues were lower than that in normal gastric mucosa.
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。
Conclusion: P53 protein can be used in early clinical diagnosis. Early in gastric carcinogenesis, its change occurs at intestinal metaplasia stage.
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。
Objective: To investigate the relationship between the development of gastric cancer and different subtypes and local patterns of intestinal metaplasia.
前言：目的：研究肠化的局部型式及不同表型与胃癌发生的关系。
Expressions of PCNA, P53, CEA are a little difference between various dysplasias and intestinal metaplasia with Sulphuric acid mucus or without Sulphuric acid mucus.
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。
Conclusion Gastroscopy and follow-up of patients with intestinal metaplasia or gastric mucosa dysplasia help to detect gastric carcinoma, especially early-stage gastric carcinoma.
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。
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.
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。
Objective: To investigate the expression of P16 protein in premalignant lesions and gastric carcinoma, including dysplastic gastric mucosa and intestinal metaplasia in gastric mucosa.
目的：研究p 16蛋白在胃癌前病变(不典型增生及肠化)及胃癌中的表达。
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.
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 %。
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