摘要
目的建立N一甲基一N’一硝基一N一亚硝基胍（N－methy1－N’－nitro－N－nitrosoguanidine，MNNG）诱发大鼠腺胃癌模型并观察p53，ras基因的表达。方法给Wistar大鼠饮用MNNG水溶液（终浓度为80μg／ml），用ABC法检测P53和P21蛋白的表达。结果MNNG成功地诱发出了胃癌、胃腺瘤、胃息肉、胃粘膜不典型增生和历上皮化生等病变。胃癌肝转移2例，淋巴结转移1例。P53蛋白在肠化及不典型增生皆阴性，胃癌阳性率为50％；P21蛋白在肠化及不典型增生中阳性率为44％，在癌组织中为23％。结论MNNG能诱发大鼠脾胃癌等病变，P53基因突变在胃癌发生发展过程中起一定作用，而ras基因激活是一个早期现象。
To study the pathogenesis of gastric cancer and investigate the p53 and H-ras genes expression incarcinogenesis and development of gastric cancer induced by MNNG. METHODS Oral administration of MNNGto Wistar rats at a concentration of 80 μg/ml in the drinking water resulted in a high incidence of tumors in theglandular stomach. p53 and p21 proteins were detected by ABC immunohistochemical method. RESULTS Adenocarcinoma. adenoma and dysplasia of the stomach were found. Two cases of metastasis of adenocarcinoma to theliver and 1 case of metastasis to the regional lymph nodes werre found. Sequential morphological studies theglandular stomach of Wistar rat receiving MNNG in the drinking water showed colonic/intestinal metaplasia anddysplasia of gastric mucosa. p21 cytoplasmic staining was seen in 44% premalignant lesions of stomach and in 24%gastric adenocarcinomas. p53 nuclear staining was seen in 50K gastric adenocarcinomas and all the premalignantlesions were negative. CONCLUSION The results suggested that p53 mutations may play a sustained role in thedevelopment of MNNG-induced adenocarcinoma of rat glandular stomach and that ras oncogenes activated the earlyevents in the induction of the gastric carcinogenic process.
出处
《中国癌症杂志》
CAS
CSCD
1998年第3期193-196,共4页
China Oncology
关键词
MNMG
动物模型
胃腺癌
基因表达
亚硝基胍
MNNG
Animal model
precancerous lesions
Gastric adenocarcinoma Oncogene expression
