Abstract
Comprehensive studies of complex recurrent translocations leading to pro-B lymphomas in repair-deficient mice demonstrate that amplification of the Myc oncogene by breakage–fusion–bridge (BFB) cycles, initiated as a consequence of site-specific nuclease-induced breaks, are a key step in the progression of this hematologic malignancy. These studies yield new insights into the mechanisms governing genome rearrangement and repair.
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