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目的探讨胃粘膜癌变过程中幽门螺杆菌(Helicobacterpylori,Hp)感染与p53,cerbB2基因表达的关系.方法浅表性胃炎16例,肠上皮化生22例,异型增生14例,早期胃癌18例及进展期胃癌40例作为研究对象.用WarthinStary银染色法检测Hp,用免疫组化Sp法检测p53和cerbB2的基因表达产物.结果Hp,p53,cerbB2在浅表性胃炎的检出率各为500%,00%,00%;在肠上皮化生的检出率各为591%,227%,136%;在异型增生的检出率各为857%,643%,286%;在早期胃癌的检出率各为167%,333%,111%;在进展期胃癌的检出率各为50%,525%,550%;在癌旁粘膜的Hp检出率为867%;在癌前病变中,Hp阳性组的p53,cerbB2表达率均高于Hp阴性组.结论Hp感染参与了胃癌前病变的发生与发展;Hp感染可引起野生型p53基因失活和cerbB2基因激活,从而导致胃粘膜的癌变.
Objective To investigate the relationship between Helicobacter pylori (Hp) infection and the expression of p53 and cerbB2 genes in gastric carcinogenesis. Methods 16 cases of superficial gastritis, 22 cases of intestinal metaplasia, 14 cases of dysplasia, 18 cases of early gastric cancer and 40 cases of advanced gastric cancer were studied. Hp was detected by Warthin-Stary silver staining and p53 and cerbB2 gene expression products were detected by immunohistochemical Sp method. Results The detection rates of Hp, p53, cerbB2 in superficial gastritis were 500%, 00%, and 00% respectively. The detection rate of intestinal metaplasia was 591. %, 22 7%, 13 6%; the detection rate of dysplasia was 85 7%, 64 3%, and 28 6% respectively; the detection rate of early-stage gastric cancer was 16 7%, respectively. 33%, 11% and 1% respectively; the detection rate of advanced gastric cancer was 50%, 52%, and 55%, respectively; the detection rate of Hp in adjacent mucosa was 86.7%. In precancerous lesions, the expression rates of p53 and cerbB2 in Hp-positive group were higher than those in Hp-negative group. Conclusion Hp infection is involved in the occurrence and development of precancerous lesions. Hp infection can lead to the inactivation of wild-type p53 gene and activation of cerbB2 gene, leading to the carcinogenesis of gastric mucosa.