Boabang P, Kurbacher C M, Waida A, Amo-Takyi B K
Department of Obstetrics and Gynecology, University of Cologne, Cologne, Germany.
Gynecol Obstet Invest. 2001;51(4):233-9. doi: 10.1159/000058056.
We analyzed tumor tissues from 14 patients with invasive squamous cell carcinoma of the cervix for aberrations of chromosome 17 and p53 expression. All but 3 patients were negative for p53 protein expression, the protein being detected in 2 International Federation of Obstetrics and Gynecology stage IIa cancers and 1 stage Ib G3 carcinoma. Significant cytogenetic aberrations in the form of losses and gains of chromosome 17 were diagnosed in 9 and 7 patients, respectively. There was no correlation with tumor prognosis, clinical stage or histologic grade. According to most reports, almost all cervical carcinomas contain integrated human papilloma virus (HPV) and express E6 oncoproteins. Increasing evidence suggests that E6 protein interaction leads to p53 mutation in HPV-infected cervical epithelium. Since most cervical tumors are infected with HPV, and the tumors originate through p53 gene mutation caused by the said interaction, which leads subsequently to the overexpression of p53 oncoprotein, lack of the latter in the remaining 11 cervical tumors may either be the result of technical shortcomings, or the tumor may arise in such circumstances through a p53-independent pathway. On the other hand, 2 of 3 stage IIa cancers and 1 Ib G3 carcinoma were found to be p53 positive, thus supporting the notion that p53 inactivation is a relatively late event in the progression of cervical cancer.
我们分析了14例宫颈浸润性鳞状细胞癌患者的肿瘤组织,以检测17号染色体畸变和p53表达情况。除3例患者外,其余患者的p53蛋白表达均为阴性,在2例国际妇产科联盟(FIGO)IIa期癌症和1例Ib期G3级癌中检测到了该蛋白。分别在9例和7例患者中诊断出以17号染色体缺失和增加形式存在的明显细胞遗传学畸变。这与肿瘤预后、临床分期或组织学分级均无相关性。根据大多数报告,几乎所有宫颈癌都含有整合型人乳头瘤病毒(HPV)并表达E6癌蛋白。越来越多的证据表明,E6蛋白相互作用会导致HPV感染的宫颈上皮细胞中p53突变。由于大多数宫颈肿瘤感染了HPV,且肿瘤是由上述相互作用导致的p53基因突变引发的,随后导致p53癌蛋白过度表达,其余11例宫颈肿瘤中缺乏该蛋白可能是技术缺陷所致,或者肿瘤可能是通过不依赖p53的途径在这种情况下发生的。另一方面,在3例IIa期癌症中有2例以及1例Ib期G3级癌被发现p53呈阳性,从而支持了p53失活是宫颈癌进展中相对较晚发生的事件这一观点。