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The genetic basis of cancer has been firmly established in the last few decades. Genomic instability is a hallmark feature of virtually all breast cancer cells, and is caused either by inherited mutations in genes that control genomic fidelity and stability (particularly in DNA repair pathways), or somatic mutations that are acquired during breast cancer progression. We originally identified translocations in 3 DNA repair genes (RAD51C, EYA2, BRIP1) in MCF7 breast cancer cells, and hypothesized that structural genomic alterations in genes that are themselves actually involved in DNA repair enhance the level of genomic instability and ultimately affect breast cancer progression and prognosis. However, we found that these translocations are specific to MCF7 cells (private mutations) and not present in any other cell lines. In addition, the RAD51C-ATXN7 fusion gene alternatively spliced and not expressed as a full length fusion gene. The short isoform wasnt found to have altered biochemical function. In summary, this study supports other recent reports in finding that DNA translocations arent recurrent in human breast cancer.