Helland A, Karlsen F, Due E U, Holm R, Kristensen G, Børresen-Dale A l
Department of Genetics, Institute of Cancer Research, Oslo, Norway.
Br J Cancer. 1998 Jul;78(1):69-72. doi: 10.1038/bjc.1998.444.
Several studies have focused on the role of p53 inactivation in cervical cancer, either by inactivating mutations in the TP53 gene or by degradation of the p53 protein by human papillomavirus (HPV). In this study, primary cervical carcinomas from 365 patients were analysed for presence of HPV using both consensus primer-sets and type-specific primer-sets. Nineteen samples were determined to have no or low virus load, and were selected for further analyses: mutation screening of the TP53 gene using constant denaturant gel electrophoresis (CDGE) followed by sequencing, and protein expression of p53, MDM2 and p21 using immunohistochemistry (IHC). Mutations in the TP53 gene were found in eight samples (42%). Elevated p53 protein expression was significantly associated with presence of a mutation (P < 0.007). P21 protein expression was detected in 16 of the 19 carcinomas. No p21 expression was seen in normal cervical tissue. Two samples, both with wild-type p53, had elevated MDM2 expression. Compared with a previous study from our group, of mainly HPV-positive cervical carcinomas, in which only one sample was found to contain a TP53 mutation, a significantly higher mutation frequency (P < 0.001) was found among the carcinomas with no or low virus load. Although p53 inactivation pathways are not detected in every tumour, our study supports the hypothesis that p53 inactivation, either by binding to cellular or viral proteins or by mutation, is essential in the development of cervical carcinomas.
多项研究聚焦于p53失活在宫颈癌中的作用,其途径包括TP53基因的失活突变或人乳头瘤病毒(HPV)介导的p53蛋白降解。在本研究中,使用共有引物组和型特异性引物组对365例患者的原发性宫颈癌进行HPV检测。确定19个样本病毒载量无或低,并选择这些样本进行进一步分析:采用恒定变性凝胶电泳(CDGE)随后测序对TP53基因进行突变筛查,以及采用免疫组织化学(IHC)检测p53、MDM2和p21的蛋白表达。在8个样本(42%)中发现了TP53基因的突变。p53蛋白表达升高与突变的存在显著相关(P < 0.007)。在19例癌组织中有16例检测到p21蛋白表达。在正常宫颈组织中未观察到p21表达。2个样本p53均为野生型,但MDM2表达升高。与我们团队之前一项主要针对HPV阳性宫颈癌的研究相比,在该研究中仅发现1个样本含有TP53突变,而在病毒载量无或低的癌组织中发现了显著更高的突变频率(P < 0.001)。尽管并非在每个肿瘤中都检测到p53失活途径,但我们的研究支持这样的假说,即p53通过与细胞或病毒蛋白结合或通过突变而失活,在宫颈癌的发生发展中至关重要。