Stratton M R, Fisher C, Gusterson B A, Cooper C S
Section of Chemical Carcinogenesis, Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
Cancer Res. 1989 Nov 15;49(22):6324-7.
Previous studies have demonstrated that genes of the ras family (H, K, and N) can be activated by point mutations at codons 12, 13, and 61. In the present study we have used oligonucleotide probes corresponding to these regions to assess the role of ras gene mutations in the genesis of human rhabdomyosarcoma. To increase the sensitivity of this method the appropriate regions of the three ras genes were first amplified using the polymerase chain reaction. The results show that 35% (5/14) embryonal rhabdomyosarcomas investigated contain mutations in the N-ras or K-ras genes. Thus ras gene mutation is implicated in the development of mesenchymal and embryonal tumors in addition to its previously documented role in epithelial and hematological neoplasia.
先前的研究表明,ras家族(H、K和N)的基因可因密码子12、13和61处的点突变而被激活。在本研究中,我们使用了与这些区域对应的寡核苷酸探针,以评估ras基因突变在人类横纹肌肉瘤发生中的作用。为提高该方法的敏感性,首先利用聚合酶链反应扩增三个ras基因的相应区域。结果显示,在所研究的14例胚胎性横纹肌肉瘤中,35%(5/14)含有N-ras或K-ras基因突变。因此,除了其先前已被证实在上皮性和血液肿瘤中所起的作用外,ras基因突变也与间叶性和胚胎性肿瘤的发生有关。