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作 者:陈立新[1] 程留芳[2] 杨云生[2] 杨少波[1] 唐晓兰[1]
机构地区:[1]解放军第304医院 [2]解放军总医院
出 处:《解放军医学杂志》2002年第3期271-272,共2页Medical Journal of Chinese People's Liberation Army
摘 要:采用聚合酶链反应 单链构象多肽性分析法 (PCR SSCP)及HP尿素酶快速检测法 ,随机对 4 6例慢性浅表性胃炎、39例慢性萎缩性胃炎、39例胃溃疡、36例胃癌的胃粘膜活检标本进行了ras、p16、p5 3及HP检测 ,并对其在胃癌致癌机制中的相互关系进行研究。结果表明 ,①ras及p5 3在胃癌标本中的检出率明显高于萎缩性胃炎、胃溃疡及浅表性胃炎 (P <0 0 5 ) ;② p16在胃癌标本中的检出率远远低于基本正常胃粘膜及其他胃良性病变 (P<0 0 5 ) ;③HP在胃癌标本中的检出率明显高于萎缩性胃炎、胃溃疡及浅表性胃炎 (P <0 0 5 ) ;④ras和p5 3阳性表达的各种胃良、恶性疾病中的HP阳性检出率均高于p16阳性表达的各种胃良、恶性疾病中的HP阳性检出率(P <0 0 5 )。提示ras、p5 3、p16和HP感染在胃癌致病机制中可能具有重要作用 。Biopsies were randomly taken from 160 patients through endoscopy. Among them 46 patients suffered from chronic superfacial gastritis, 39 patients from chronic atrophic gastritis, 39 patients from gastric ulcer, and 36 patients from gastric cancer. Ras, p16, and p53 genes were analysed with polymerase chain reaction single strand conformation polymorphism (PCR SSCP). Helicobacter pylori (HP) was examined with RUT. Result: ① the positive rates of ras and mutant p53 in gastric cancer were significantly higher than that in gastritis and gastric ulcer( P <0 05); ② the detection rate of p16 gene in gastric cancer was significantly lower than that in normal gastric mucosa ( P <0 01) and gastric benign diseases ( P <0 05); ③ the positive rate of HP was significantly higher in gastric cancer than in chronic superficial gastritis, chronic atrophic gastritis and gastric ulcer ( P <0 05); ④The expressions of ras and p53 in the biopsies of gastric cancer and chronic atrophic gastritis with HP were higher than those of chronic superficial gastritis and gastric ulcer with HP, but the expression of p16 was lower in gastric cancer patients with HP than in patients with chronic superficial gastritis and chronic atrophic gastritis with HP ( P <0 05). The above results show that gastric cancer genesis or development may be related with the activation of ras,mutation of p53 oncogenes or deletion of p16 tumor suppressor genes, and that HP is an important factor in the pathogenesis of gastric cancer. Ras, p16,p53 and HP may interact in the carcinogenesis of gastric mucosa.
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