Garte S J, Burns F J
Department of Environmental Medicine, New York University Medical Center, NY 10016.
Environ Health Perspect. 1991 Jun;93:45-9. doi: 10.1289/ehp.919345.
Current research indicates a role for several oncogenes in radiation-induced carcinogenesis in vivo and cell transformation in vitro. Certain oncogenes are probably also involved in some cases of human cancer caused by exposure to nonionizing radiation and may play a mechanistic role in the phenomenon of radioresistance seen in later stages of tumor progression. The mechanisms of oncogene activation seen in radiation-induced tumors include point mutations, gene amplification, and changes in gene expression. Genetic factors associated with target species, strain, and tissue type play an important role in determining the specific nature of oncogene activation by radiation exposure. Using the rat skin as a model for cancer induction by ionizing radiation, we found concurrent activation of K-ras and c-myc oncogenes in end-stage tumors. Amplification of the myc gene proved to occur during a late stage of tumor progression and is not an early initiating event resulting from the direct action of radiation on target cells. The importance of tissue specificity, tumor cell heterogeneity, and physical characteristics of the radiation exposure are discussed.
当前研究表明,几种癌基因在体内辐射诱导的致癌作用以及体外细胞转化中发挥作用。某些癌基因可能也参与了一些因接触非电离辐射导致的人类癌症病例,并且可能在肿瘤进展后期出现的放射抗性现象中发挥机制性作用。在辐射诱导的肿瘤中观察到的癌基因激活机制包括点突变、基因扩增和基因表达变化。与靶物种、品系和组织类型相关的遗传因素在确定辐射暴露导致癌基因激活的具体性质方面起着重要作用。以大鼠皮肤作为电离辐射诱导癌症的模型,我们发现在晚期肿瘤中K-ras和c-myc癌基因同时被激活。myc基因的扩增被证明发生在肿瘤进展的后期,而不是辐射对靶细胞直接作用导致的早期起始事件。本文还讨论了组织特异性、肿瘤细胞异质性以及辐射暴露的物理特征的重要性。