作者在1975年～1979年调查了596例视网膜母细胞瘤(RB)病人。细胞遗传学分析发现,定位在13ql4的Rb-1基因缺失可引起RB,由于抑制(或控制)这种基因的功能失活而导致癌基因激活。另一方面,癌基因激活常与染色体异常或基因扩增有关。以前曾报道在RB肿瘤细胞系和RB肿瘤组织细胞中出现N-myc癌基因扩增并证明与双微体(DM)及均质染色区(HSR)有密切关系。作者进一步研究了RB肿瘤癌基因激活和染色体异常之间的关系,并考虑到肿瘤类型和家族背景。取正常人的肝、脾及皮肤成纤维细胞的N-myc作为标准。扩增超过 The authors investigated 596 patients with retinoblastoma (RB) from 1975 to 1979. Cytogenetic analysis revealed that deletion of the Rb-1 gene located in 13ql4 caused RB activation, which resulted in the oncogene activation due to inhibition (or control) of the inactivation of this gene. On the other hand, oncogene activation is often associated with chromosomal abnormalities or gene amplification. N-myc oncogene amplification has been previously reported in RB tumor cell lines and RB tumor tissue cells and has been shown to be closely related to the double microsomes (DM) and the homogenously stained zone (HSR). The authors further studied the relationship between RB tumor oncogene activation and chromosomal abnormalities, taking into account the tumor type and family background. N-myc was taken as standard for normal human liver, spleen, and skin fibroblasts. Amplification exceeds