Nanus D M, Mentle I R, Motzer R J, Bander N H, Albino A P
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021.
J Urol. 1990 Jan;143(1):175-8. doi: 10.1016/s0022-5347(17)39905-6.
The role of ras oncogenes in the pathogenesis of renal cell carcinoma is unclear. We have previously shown that insertion of a mutated ras oncogene into cultured human proximal tubular cells, the normal counterpart of renal cell carcinomas, initiates a series of transformation events which results in cells possessing a renal cancer phenotype. These data suggested a role for mutated ras genes in the initiation and maintenance of this disease. Therefore, to assess the involvement of ras genes in renal carcinogenesis, 51 primary and metastatic renal carcinomas, including three oncocytomas, were analyzed for point mutations in codons 12, 13 and 61 of the Ha-ras, Ki-ras and N-ras proto-oncogenes using polymerase-catalyzed chain reaction methodology. A mutated Ha-ras gene was found in one renal cancer metastatic to lung for an overall incidence of 2%. These data indicate that ras oncogenes, activated by point mutations, do not play a major role in the initiation, maintenance or metastases of renal carcinomas.
ras癌基因在肾细胞癌发病机制中的作用尚不清楚。我们之前已经表明,将一个突变的ras癌基因插入培养的人近端肾小管细胞(肾细胞癌的正常对应细胞)中,会引发一系列转化事件,导致细胞具有肾癌表型。这些数据表明突变的ras基因在这种疾病的起始和维持中发挥作用。因此,为了评估ras基因在肾癌发生中的作用,我们使用聚合酶催化链反应方法,对51例原发性和转移性肾癌(包括3例嗜酸细胞瘤)的Ha-ras、Ki-ras和N-ras原癌基因的第12、13和61密码子的点突变进行了分析。在一例转移至肺部的肾癌中发现了一个突变的Ha-ras基因,总发生率为2%。这些数据表明,由点突变激活的ras癌基因在肾癌的起始、维持或转移中不发挥主要作用。