Färber B, Kinzel V
Institute of Experimental Pathology, German Cancer Research Center, Heidelberg.
Carcinogenesis. 1990 Nov;11(11):2067-70. doi: 10.1093/carcin/11.11.2067.
In order to gain further insight into the mechanism of clastogenic action of the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA), the localization and distribution of structural chromosomal aberrations on HeLa chromosomes was investigated. We have shown by the G-banding technique that TPA-induced chromosomal aberrations in HeLa cells have practically the same distribution as that occurring spontaneously in control cultures. About two-thirds of the breakpoints are located in areas of known fragile sites; about one-third is located in regions near known oncogenes. The tumor promoter TPA thus appears to enhance pre-existing mechanisms of an 'endogeneous' clastogenesis.
为了进一步深入了解佛波酯12-O-十四烷酰佛波醇-13-乙酸酯(TPA)的致断裂作用机制,研究了HeLa染色体上结构性染色体畸变的定位和分布。我们通过G显带技术表明,TPA诱导的HeLa细胞染色体畸变的分布与对照培养物中自发出现的分布几乎相同。大约三分之二的断点位于已知脆性位点区域;大约三分之一位于已知癌基因附近的区域。因此,肿瘤启动子TPA似乎增强了“内源性”断裂发生的预先存在的机制。