Mouw Kent W, D'Andrea Alan D
Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States; Harvard Radiation Oncology Program, Boston, MA, United States.
Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States.
DNA Repair (Amst). 2014 Jul;19:130-4. doi: 10.1016/j.dnarep.2014.03.019. Epub 2014 Apr 24.
Cells have evolved multiple distinct DNA repair pathways to efficiently correct a variety of genotoxic lesions, and decades of study have led to an improved understanding of the mechanisms and regulation of these individual pathways. However, there is now an increasing appreciation that extensive crosstalk exists among DNA repair pathways and that this crosstalk serves to increase the efficiency and diversity of response to damage. The Fanconi anemia (FA)/BRCA and nucleotide excision repair (NER) pathways have been shown to share common factors, and often work in concert to repair damage. Genomic studies are now revealing that many tumors harbor somatic mutations in FA/BRCA or NER genes, which may provide a growth advantage, but which could also be exploited therapeutically.
细胞已经进化出多种不同的DNA修复途径，以有效地纠正各种基因毒性损伤，数十年的研究使人们对这些个体途径的机制和调控有了更好的理解。然而，现在人们越来越认识到，DNA修复途径之间存在广泛的相互作用，并且这种相互作用有助于提高对损伤反应的效率和多样性。范可尼贫血（FA）/BRCA和核苷酸切除修复（NER）途径已被证明有共同的因子，并且经常协同作用来修复损伤。基因组研究现在表明，许多肿瘤在FA/BRCA或NER基因中存在体细胞突变，这可能提供生长优势，但也可以用于治疗。
