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BRCA2  encodes a protein with a fundamental role in homologous recombination that is essential for normal development. Carrier status of mutations  in BRCA2  is associated with familial breast and ovarian cancer, while bi-allelic  BRCA2  mutations can cause Fanconi anemia (FA), a cancer predisposition syndrome with cellular cross-linker hypersensitivity. Cancers associated with  BRCA2  mutations can acquire chemo-resistance on relapse. We modeled acquired cross-linker resistance with an FA-derived  BRCA2- mutated acute myeloid leukemia (AML) platform. Associated with acquired cross-linker resistance was the expression of a functional BRCA2 protein variant lacking exon 5 and exon 7 ( BRCA2   ΔE5+7  ), implying a role for  BRCA2  splicing for acquired chemo-resistance. Integrated network analysis of transcriptomic and proteomic differences for phenotyping of BRCA2 disruption infers impact on transcription and chromatin remodeling in addition to the DNA damage response. The striking overlap with transcriptional profiles of FA patient hematopoiesis and  BRCA  mutation associated ovarian cancer helps define and explicate the ‘ BRCAness’  profile.

Acquired cross-linker resistance associated with a novel spliced BRCA2 protein variant for molecular phenotyping of BRCA2 disruption