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The Fanconi anemia (FA) pathway plays a central role in the repair of DNA interstrand crosslinks (ICLs) and regulates cellular responses to replication stress. Homologous recombination (HR), the error-free pathway for double-strand break (DSB) repair, is required during physiological cell cycle progression for the repair of replication-associated DNA damage and protection of stalled replication forks. Substantial crosstalk between the two pathways has recently been unravelled, in that key HR proteins such as the RAD51 recombinase and the tumour suppressors BRCA1 and BRCA2 also play important roles in ICL repair. Consistent with this, rare patient mutations in these HR genes cause FA pathologies and have been assigned FA complementation groups. Here, we focus on the clinical and mechanistic implications of the connection between these two cancer susceptibility syndromes and on how these two molecular pathways of DNA replication and repair interact functionally to prevent genomic instability.

Original publication

DOI

10.15252/embj.201693860

Type

Journal article

Journal

EMBO J

Publication Date

02/05/2016

Volume

35

Pages

909 - 923

Keywords

DNA damage response, DNA repair, Fanconi anemia, genome stability, homologous recombination, replication stress, DNA Repair, DNA Repair Enzymes, Fanconi Anemia Complementation Group Proteins, Genetic Predisposition to Disease, Homologous Recombination, Humans, Metabolic Networks and Pathways, Neoplasms