<p>DNA breakage at specific rearrangement-participating genes, which are more sensitive to a range of environmental and chemotherapeutic agents than other regions of the human genome, contributes to the generation of leukemia-causing rearrangements, and can be used as a predictor of susceptibility to cancer caused by gene rearrangements. As a direct proof-of-principle regarding the feasibility of employing fragile site breakage to identify and monitor high-risk populations to allow personalized treatments, genome-wide DNA break mapping/sequencing was used to determine whether preferential DNA breaks are generated at the major breakpoint regions of KMT2A in AML remission patients with previously diagnosed KMT2A rearrangement.  We are submitting break mapping data from three patients with KMT2A rearrangements and three non-fusion patients, with and without etoposide treatments.</p>

DNA Double Strand Breaks in KMT2A-Rearranged AML patients

Assessing acute myeloid leukemia susceptibility in rearrangement‐driven patients by DNA breakage at topoisomerase II and CCCTC‐binding factor/cohesin binding sites