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• W2127999710 abstract "MLL gene fusions are the hallmark of more than 70% of therapy-related leukemias (t-ML) associated with topoisomerase II inhibitors (e.g., etoposide) and cause leukemia in murine transgenic models. To determine whether Mll genomic fusions can occur after exposure to topoisomerase II inhibitors, we developed a long-distance inverse PCR DNA-based assay for chimeric Mll fusions in mouse embryonic stem cells. We detected Mll fusions at a higher frequency following 100 µM etoposide for 8 h (16×10‒6 cell−1) than in no-drug controls (1.0×10‒6 cell−1, P=0.0002) or after treatment with a comparably cytotoxic exposure to the antimicrotubule drug vincristine (1.0×10‒6 cell-1, P=0.0047). The fusion points in Mll chimeric products induced by etoposide were localized to a 1.5 kb region between exons 9 and 11, analogous to the MLL breakpoint cluster region in human leukemia. All 49 Mll fusion partners analyzed matched known genomic murine sequences, with 40 (82%) matching annotated genes covering eighteen murine autosomes. One partner was Runxl, the murine homologue of the transcription factor AML-l, a target of human translocations in therapy-related leukemia. These findings indicate that etoposide triggers the formation of Mll gene fusions, a critical step for the development of treatment-induced leukemic transformation." @default.
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• W2127999710 date "2003-11-20" @default.
• W2127999710 modified "2023-09-25" @default.
• W2127999710 title "Etoposide induces chimeric <i>Mll</i> gene fusions" @default.
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• W2127999710 doi "https://doi.org/10.1096/fj.03-0638fje" @default.
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