Crosstalk between the nucleotide excision repair and Fanconi anemia/BRCA pathways.
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.
Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States; Harvard Radiation Oncology Program, Boston, MA, United States.
Kent W
KW
Mouw
Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States. Electronic address: alan_dandrea@dfci.harvard.edu.
Alan D
AD
D'Andrea
D019313:BRCA1 Protein / Q000235:genetics / Q000378:metabolism; D024682:BRCA2 Protein / Q000235:genetics / Q000378:metabolism; D002453:Cell Cycle / Q000235:genetics*; D004249:DNA Damage / Q000235:genetics; D004260:DNA Repair / Q000235:genetics*; D005199:Fanconi Anemia / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D018095:Germ-Line Mutation; D006801:Humans; D015398:Signal Transduction / Q000235:genetics*
D019313:BRCA1 Protein; D024682:BRCA2 Protein; C551750:BRCA2 protein, human
BRCA; Crosslink repair; Fanconi anemia; Nucleotide excision repair; PARP inhibitor