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本文收集的60例活检宫颈癌组织,对同一病例同时进行HPV、C-myc、H-ras和P~(53)对比研究发现85％的组织中感染HPV,尤其是HPV_(16)和HPV_(18)(78.43％与21.56％),表明HPV_(18)和HPV_(16)作为宫颈癌病因依据是充分的,但不是唯一因素。在癌基因研究中,C—myc扩增率比H—ras高(33％与6.6％),C—myc扩增在HPV感染阳性组织中占89.47％,而HPV_(16)占76.5％;HPV_(18)仅占11.8％,表明HPV DNA,尤其是HPV_(16)DNA对细胞基因的整合而激活C—myc原癌基因,起到了一定的协同致癌作用。C—myc及H—ras癌基因扩增和重排与P~(53)基因杂合性丢失似无关,而P~(53)基因杂合性丢失率在HPV感染阴性组织中比阳性组织高(89％与7.8％),提示P~(53)基因杂合性丢失与HPV感染无明显关。而未被HPV感染的宫颈癌组织中野生型P~(53)基因丢失可能是导致癌瘤的关键。
In this study, 60 cases of biopsy cervical cancer tissues were collected and HPV, C-myc, H-ras and P53 were detected simultaneously in the same case. HPV was found in 85% of the cases, especially HPV16 and HPV_ 18) (78.43% vs 21.56%), indicating that HPV 18 and HPV 16 are sufficient, but not the only factors for the etiology of cervical cancer. In oncogenes, C-myc was higher than that of H-ras (33% vs 6.6%), C-myc was 89.47% in HPV-positive tissues and 76.5% (18) accounted for only 11.8%, indicating that HPV DNA, especially HPV16 (16) DNA on cell gene integration and activation of C-myc oncogene, played a certain role in carcinogenesis. The amplification and rearrangement of C-myc and H-ras oncogenes were not related to the loss of P53 gene heterozygosity, whereas the loss of heterozygosity for P53 gene was higher in HPV-negative than in positive (89% vs 7.8%), suggesting that loss of heterozygosity of P ~ (53) gene was not related to HPV infection. However, the loss of wild-type P53 gene in cervical cancer tissues without HPV infection may be the key factor leading to carcinogenesis.