Abstract：
The DNA is constantly under attack from endogenous and exogenous damaging agents. The damaged DNA must be repaired quickly to avoid genomic instability and to prevent the occurrence of a malignant transformation. Once a lesion is detected, the DNA repair mechanism initiates and replaces the structurally altered base or any other abnormality. The cell repair mechanisms include direct reversal, excision repair (base excision repair [BER] and nucleotide excision repair [NER]), mismatch repair (MMR), homologous recombination repair (HR) and non-homologous end joining (NHEJ). Unrepaired DNA could lead to mutation, cell death or cancer. This review will discuss how the defects in DNA repair play a vital role in cancer initiation, development and progression.
摘要：
DNA不断受到内源性和外源性损伤剂的攻击。必须快速修复受损的DNA以避免基因组不稳定并防止恶性转化的发生。一旦检测到病变，DNA修复机制启动并取代结构改变的碱基或任何其他异常。细胞修复机制包括直接逆转，切除修复（碱基切除修复[BER]和核苷酸切除修复[NER]），失配修复(MMR),同源重组修复（HR）和非同源末端连接（NHEJ）。未修复的DNA会导致突变,细胞死亡或癌症。这篇综述将讨论DNA修复缺陷如何在癌症发生中起重要作用。发展和进步。
