Rochlitz C F, Peter S, Willroth G, de Kant E, Lobeck H, Huhn D, Herrmann R
Abt. Hämatologie/Onkologie, Klinikums Charlottenburg, Freien Universität Berlin, F.R.G.
Eur J Cancer. 1992;28(2-3):333-6. doi: 10.1016/s0959-8049(05)80048-6.
Mutations in codon 12, 13 or 61 of one of the three ras genes, Ha-ras, Ki-ras, and N-ras, convert these genes into active oncogenes. To determine the role mutated ras genes play in the carcinogenesis of renal cell carcinoma, we analysed tumour DNA and unaffected renal tissue derived from 55 patients. The polymerase chain reaction technique was used to amplify DNA fragments containing Ki-, Ha-, and N-ras codons 12, 13, and 61. The amplified fragments were then probed on slot-blots with labeled mutation-specific oligomers. A single Ki-ras mutation (codon 12, gly- greater than val) was detected in a patient with a pT2N2M1 tumour. We concluded that ras oncogene mutations do not play an important role in the initiation of renal cell carcinoma.
三种ras基因(Ha-ras、Ki-ras和N-ras)之一的第12、13或61密码子发生突变,会将这些基因转变为活性癌基因。为了确定突变的ras基因在肾细胞癌致癌过程中所起的作用,我们分析了来自55例患者的肿瘤DNA和未受影响的肾组织。采用聚合酶链反应技术扩增包含Ki-、Ha-和N-ras基因第12、13和61密码子的DNA片段。然后用标记的突变特异性寡聚物在狭缝印迹上对扩增片段进行检测。在一名患有pT2N2M1肿瘤的患者中检测到一个单一的Ki-ras突变(第12密码子,甘氨酸突变为缬氨酸)。我们得出结论,ras癌基因突变在肾细胞癌的起始过程中不发挥重要作用。