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The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses.

Original publication




Journal article


Nat Struct Mol Biol

Publication Date





755 - 757


Antineoplastic Agents, BRCA2 Protein, Cell Line, Tumor, Cell Survival, DNA Damage, DNA Replication, Fanconi Anemia Complementation Group D2 Protein, Genome, Human, Genomic Instability, HEK293 Cells, Humans, Phthalazines, Piperazines