Iwasaka T, Oh-uchida M, Matsuo N, Yokoyama M, Fukuda K, Hara K, Fukuyama K, Hori K, Sugimori H
Department of Obstetrics and Gynecology, Saga Medical School, Japan.
Gynecol Oncol. 1993 Jan;48(1):104-9. doi: 10.1006/gyno.1993.1016.
Human papillomavirus (HPV) infection is clearly associated with cervical carcinomas, yet it is also true that there are cervical carcinomas in which HPV DNA is absent. We examined eight established cell lines derived from cervical carcinomas for the presence of mutations of the p53 antioncogene in relation to the presence of HPV DNA sequences. Of these eight cell lines, seven were positive for HPV DNA and the remaining one was negative for HPV DNA. Single-strand conformation polymorphism analyses revealed a point mutation of the p53 gene in the cell line in which HPV DNA was absent. Sequencing analysis revealed a single-base mutation at codon 273 from CGT to CAT(Arg-->His) and immunocytochemical studies provided evidence that the p53 protein was overexpressed in this cell line. Our observations suggest that the loss of normal p53 gene function may be linked to the oncogenesis of cervical carcinoma.
人乳头瘤病毒（HPV）感染显然与宫颈癌有关，但确实也存在一些不存在HPV DNA的宫颈癌。我们检测了8种源自宫颈癌的成熟细胞系，以研究p53抗癌基因的突变情况与HPV DNA序列存在与否的关系。在这8种细胞系中，7种HPV DNA呈阳性，其余1种HPV DNA呈阴性。单链构象多态性分析显示，在不存在HPV DNA的细胞系中p53基因存在点突变。测序分析显示，密码子273处发生了从CGT到CAT（精氨酸→组氨酸）的单碱基突变，免疫细胞化学研究提供的证据表明该细胞系中p53蛋白过度表达。我们的观察结果表明，正常p53基因功能的丧失可能与宫颈癌的发生有关。
