Livingstone L R, White A, Sprouse J, Livanos E, Jacks T, Tlsty T D
Lineberger Comprehensive Cancer Center, Department of Pathology, University of North Carolina, School of Medicine, Chapel Hill 27599-7295.
Cell. 1992 Sep 18;70(6):923-35. doi: 10.1016/0092-8674(92)90243-6.
Gene amplification occurs at high frequency in transformed cells (10(-3)-10(-5)), but is undetectable in normal diploid fibroblasts (less than 10(-9)). This study examines whether alterations of one or both p53 alleles were sufficient to allow gene amplification to occur. Cells retaining one wild-type p53 allele mimicked the behavior of primary diploid cells: they arrested growth in the presence of drug and failed to demonstrate amplification. Cells losing the second p53 allele failed to arrest when placed in drug and displayed the ability to amplify at a high frequency. Thus, loss of wild-type p53 may lead to amplification, possibly caused by changes in cell cycle progression. Other determinants can by-pass this p53 function, however, since tumor cells with wild-type p53 have the ability to amplify genes.
基因扩增在转化细胞中高频发生(10^(-3)-10^(-5)),但在正常二倍体成纤维细胞中无法检测到(小于10^(-9))。本研究检测一个或两个p53等位基因的改变是否足以使基因扩增发生。保留一个野生型p53等位基因的细胞模拟原代二倍体细胞的行为:它们在药物存在下停止生长,且未表现出扩增。失去第二个p53等位基因的细胞在置于药物中时未停止生长,并表现出高频扩增的能力。因此,野生型p53的缺失可能导致扩增,这可能是由细胞周期进程的改变引起的。然而,其他决定因素可以绕过这种p53功能,因为具有野生型p53的肿瘤细胞有扩增基因的能力。