Cazaux C
Université Paul-Sabatier, Université de Toulouse, Toulouse Cedex 04, France.
Bull Cancer. 2010 Nov;97(11):1241-51. doi: 10.1684/bdc.2010.1202.
Genomic DNA displays a non canonical structure prone to be damaged and modified by genotoxic stresses, which are induced either by the endogenous metabolism or attacks from environment or therapeutic pressure. Several molecular pathways allow cells to repair such DNA lesions. Additional mechanisms have been selected to bypass such damage at the price of mutations. The maintenance of the genome is thus mediated by the respect of a balance between accurate and inaccurate DNA transactions. This review deals with the tumor suppressor role of such equilibrium, as well as the impact of an unbalance on carcinogenesis.
基因组DNA呈现出一种非经典结构，容易受到基因毒性应激的损伤和修饰，这些应激是由内源性代谢、环境攻击或治疗压力所诱导的。几种分子途径使细胞能够修复此类DNA损伤。还选择了其他机制以突变的代价绕过此类损伤。因此，基因组的维持是通过在准确和不准确的DNA交易之间保持平衡来介导的。本综述探讨了这种平衡的肿瘤抑制作用，以及失衡对致癌作用的影响。
