Garte S J, Burns F J, Ashkenazi-Kimmel T, Felber M, Sawey M J
New York University Medical Center, Institute of Environmental Medicine, New York 10016.
Cancer Res. 1990 May 15;50(10):3073-7.
Evaluation of a large panel of radiation-induced rat skin tumors of diverse size and histological type revealed a correlation between c-myc copy number and tumor size. Both the frequency and degree of c-myc gene amplification were increased in large compared to small carcinomas, but none of the sarcomas examined showed c-myc amplification. Serial biopsies of individual tumors exhibited similar trends of increasing c-myc copy number in later biopsies. In one regressing tumor, the c-myc gene copy number paralleled the growth rate of the tumor during growth and regression. The average time required from tumor appearance to significant gene amplification was close to the average period between tumor appearance and the onset of rapid growth. The data suggest that, rather than being a target gene for the direct early effects of ionizing radiation, c-myc functions as a late-stage progression-related oncogene in this model system.
对一大组不同大小和组织学类型的辐射诱导大鼠皮肤肿瘤进行评估后发现，c-myc拷贝数与肿瘤大小之间存在相关性。与小癌相比，大癌中c-myc基因扩增的频率和程度均有所增加，但所检查的肉瘤均未显示c-myc扩增。对单个肿瘤进行的系列活检显示，在后期活检中c-myc拷贝数有类似的增加趋势。在一个消退的肿瘤中，c-myc基因拷贝数在肿瘤生长和消退过程中与肿瘤生长速率平行。从肿瘤出现到显著基因扩增所需的平均时间接近肿瘤出现到快速生长开始之间的平均时间。数据表明，在该模型系统中，c-myc并非电离辐射直接早期效应的靶基因，而是作为一个与晚期进展相关的癌基因发挥作用。
