Yuasa Y, Kamiyama T, Kato M, Iwama T, Ikeuchi T, Tonomura A
Department of Hygiene and Oncology, School of Medicine, Tokyo Medical and Dental University, Japan.
Oncogene. 1990 Apr;5(4):589-96.
We tried to detect oncogenes associated with familial adenomatous polyposis by a tumorigenicity assay in nude mice. One polyp and two peripheral blood lymphocyte DNAs out of 12 samples from patients induced Alu-positive tumors. Lymphocyte DNAs from one of 5 healthy people also showed tumorigenic activity. The transforming genes of polyps from a patient and lymphocytes from a normal person were found to be the human N-ras gene. Since these N-ras genes were amplified in nude mouse tumors and did not show any alterations in the nucleotide sequences around codons 12 and 61, it is likely that the tumors were induced by the amplified normal N-ras genes. The transforming sequences from two patients' lymphocytes did not hybridize with 12 known oncogene probes, suggesting that these two genes are novel oncogenes or genes for which we have not yet examined the homology. One oncogene derived from a patient's lymphocytes was partially cloned and shown to be located on human chromosome 7. This gene did not hybridize with the met and erbB1 genes, which are potential oncogenes located on chromosome 7. These data indicate that this gene is a new oncogene.
我们试图通过在裸鼠中进行致瘤性试验来检测与家族性腺瘤性息肉病相关的致癌基因。在来自患者的12个样本中，有1个息肉和2个外周血淋巴细胞DNA诱导出了Alu阳性肿瘤。5名健康人中的1人的淋巴细胞DNA也显示出致瘤活性。发现1名患者息肉的转化基因和1名正常人淋巴细胞的转化基因均为人N-ras基因。由于这些N-ras基因在裸鼠肿瘤中发生了扩增，并且在密码子12和61周围的核苷酸序列中未显示任何改变，因此这些肿瘤很可能是由扩增的正常N-ras基因诱导产生的。来自2名患者淋巴细胞的转化序列与12种已知致癌基因探针均未杂交，这表明这两个基因是新的致癌基因或我们尚未检测其同源性的基因。从1名患者淋巴细胞中获得的1个致癌基因被部分克隆，并显示位于人类7号染色体上。该基因与位于7号染色体上的潜在致癌基因met和erbB1基因均未杂交。这些数据表明该基因是一个新的致癌基因。
