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应用核酸分子杂交、PCR、PCR-ASO杂交等技术,对人宫颈癌中Ha-ras等三种癌基因、HPV16病毒基因及P53、Rb抑癌基因等多基因变化及其致癌机理进行了研究。结果表明:①宫颈癌中存在Ha-ras第12位密码子G→T点突变,突变率为18.2%(8/44),并有Ha-ras基因扩增,扩增率为45%(9/20);②c-erbB2基因在宫颈癌中的扩增率为73.3%(11/15),5例伴有重排;③c-myc基因在宫颈癌中的扩增率为91.7%(11/12);④HPV16E6/E7为引物的PCR检测结果,宫颈癌中的阳性率为80.5%(33/41);⑤12例宫颈癌中未发现P58、Rb基因缺失。上述多基因致癌机理的研究表明,人宫颈癌中Ha-ras、c-myc、c-erbB2经点突变、扩增、重排而被激活,在癌变中起着协同致癌作用。HPV16基因的整合可能启动c-myc,为癌变的起始因素,而Ha-ras、c-erbB2的基因改变可能为中、晚期事件,抑癌基因P53、Rb的作用尚需进一步研究。
By using nucleic acid molecular hybridization, PCR and PCR-ASO hybridization, we investigated the multi-gene changes of Ha-ras and other oncogenes, HPV16, P53 and Rb tumor suppressor genes and their carcinogenicity in human cervical cancer. The results showed that: (1) There was a G → T point mutation in codon 12 of Ha-ras in cervical cancer, with a mutation rate of 18.2% (8/44) and a Ha-ras gene amplification rate of 45% (9/20); ② The amplification rate of c-erbB2 gene in cervical cancer was 73.3% (11/15), and 5 cases with rearrangement; ③c-myc gene amplification rate in cervical cancer was 91 .7% (11/12); ④HPV16E6 / E7 was the result of PCR, the positive rate was 80.5% (33/41) in cervical cancer; ⑤P58 and Rb were not found in 12 cases of cervical cancer. The above study of multi-gene oncogenic mechanism shows that human cervical cancer Ha-ras, c-myc, c-erbB2 point mutation, amplification, rearrangement is activated, plays a role in cancer carcinogenesis. The integration of HPV16 gene may activate c-myc, which is the initiation factor of carcinogenesis. However, the gene changes of Ha-ras and c-erbB2 may be intermediate and late events. The role of tumor suppressor genes P53 and Rb needs further study.