Kamel D, Pääkkö P, Pöllänen R, Vähäkangas K, Lehto V P, Soini Y
Department of Pathology, University of Oulu, Finland.
APMIS. 1995 May;103(5):331-8. doi: 10.1111/j.1699-0463.1995.tb01116.x.
In this study we analysed 47 bladder carcinomas for the presence of DNA-HPV subtypes 6, 11, 16, 18, 31 and 33 by nucleic acid in situ hybridization, and for the abnormal accumulation of p53 protein by immunohistochemistry. HPV DNA was found in 27/47 (57%) bladder carcinomas, with multiple subtypes in 20 cases. In squamous cell carcinoma (SCC), HPV DNA was only detected in the superficial layer of the neoplastic epithelium and was found mainly in the nuclear compartment. In contrast, in transitional cell carcinoma (TCC), HPV DNA was also found in deeper parts of the tumour. In about half the cases it was mainly found in the cytoplasmic compartment. In SCC, the HPV DNA labelling occurred in koilocytic cells, while no such association was found in TCC. Abnormal accumulation of p53 protein was found in 24/47 (51%) carcinomas. p53 positivity was found significantly more often in SCC than in TCC (p = 0.05). Concurrent HPV positivity and abnormal p53 protein accumulation was found in 18 cases, 14 showing the presence of HPV subtypes 16 and/or 18 DNA. The results demonstrate that HPV DNA occurs widely in urinary tract tumours. Unlike in some other carcinomas, there was no inverse relationship between HPV positivity and abnormal p53 protein accumulation in bladder carcinomas. Thus HPV infection may play a role in the pathogenesis of bladder carcinomas by some mechanism other than inactivation of the p53 protein.
在本研究中，我们通过核酸原位杂交分析了47例膀胱癌中DNA - HPV亚型6、11、16、18、31和33的存在情况，并通过免疫组织化学分析了p53蛋白的异常积聚情况。在47例膀胱癌中，27例（57%）检测到HPV DNA，其中20例为多种亚型。在鳞状细胞癌（SCC）中，HPV DNA仅在肿瘤上皮的表层检测到，且主要位于细胞核内。相比之下，在移行细胞癌（TCC）中，HPV DNA也在肿瘤的深部发现。约半数病例中，HPV DNA主要位于细胞质内。在SCC中，HPV DNA标记出现在挖空细胞中，而在TCC中未发现这种关联。47例癌中有24例（51%）发现p53蛋白异常积聚。SCC中p53阳性率显著高于TCC（p = 0.05）。18例同时存在HPV阳性和p53蛋白异常积聚，其中14例显示存在HPV亚型l6和/或18 DNA。结果表明，HPV DNA在尿路肿瘤中广泛存在。与其他一些癌症不同，膀胱癌中HPV阳性与p53蛋白异常积聚之间不存在负相关。因此，HPV感染可能通过p53蛋白失活以外的其他机制在膀胱癌的发病机制中起作用。
