摘要
背景与目的:研究幽门螺杆菌L型(Hp-L型)感染与胃癌浸润和转移的关系。材料与方法:应用革兰染色、透射电镜和免疫组化SP法检测130例胃癌患者手术切除的肿瘤组织标本和50例癌旁(正常)组织的Hp-L型感染及血管内皮生长因子(VEGF)、基质金属蛋白酶-2(MMP-2)的表达。分别比较胃癌组织Hp-L型感染阳性组和阴性组上述指标的表达结果,分析Hp-L型感染与胃癌浸润和转移的关系。结果:130例胃癌组织标本中免疫组化及革兰染色Hp-L型同时阳性的病例有88例,胃癌组织的Hp-L型阳性率(67.69%)明显高于对照组(24%)(P<0.05);透射电镜观察Hp-L型位于癌细胞胞质内及癌细胞间质。胃癌组织中VEGF和MMP-2表达阳性率均明显高于对照组(P<0.01);Hp-L型阳性组的MMP-2、VEGF表达阳性率也均高于Hp-L型阴性组(P<0.05);且Hp-L型阳性与VEGF和MMP-2的表达阳性均呈正相关(r=0.45,r=0.30,P均<0.01)。胃癌中Hp-L型阳性率与肿瘤的大小无关,但与癌细胞的浸润深度、局部和远处淋巴结转移相关。结论:Hp-L型感染与胃癌的发生密切相关,可能是影响胃癌浸润和转移的重要因素之一。
BACKGROUND AND AIM：To investigate the correlation between infection of helicobacter pylori L-form（Hp-L） and invasion and metastasis of gastric carcinoma.MATERIALS AND METHODS：Infection of Hp-L was examined on 130 patients with gastric carcinoma and control group by Gram staining,immunohistochemical stain（SP method） and transmission electron microscopy.Immunohistochemical stain was used for measuring the protein expressions of VEGF and MMP-2 in 180 cases of gastric carcinoma and control group.RESULTS：The rate of Hp-L infection in gastric carcinoma was 67.69% （P 〈 0.05） .Compared with the control group, the positive rate of Hp-L form in gastric carcinoma group was notably high. The difference in the positive rates of VEGF and MMP-2 expressions between gastric carcinoma and control group was obvious （P 〈 0.01）.There was a definite correlation between infection of Hp-L and the expression of VEGF and MMP-2 （P 〈 0.05） . The positive rate of Hp-L in the gastric carcinoma group correlated with depth of invasion, metastasis to the paragastric and distant lymph nodes （P 〈 0.01） but not tumor size. CONCLUSION： Hp-L infection correlated with the occurrence and progression of gastric carcinoma, and may be an important promoting factor in gastric carcinoma growth, invasion and metastasis.
出处
《癌变·畸变·突变》
CAS
CSCD
2009年第5期384-387,共4页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
安徽省教育厅高校省级自然科学研究重点项目(KJ2007A098)
蚌埠市科技局2007年第一批科技项目(11)
关键词
胃癌
幽门螺杆菌L型
浸润转移
MMP-2
gastric carcinoma
helicobacter pylori
L-form
invasion and metastasis
MMP-2
