TY - JOUR T1 - Therapy-induced Deletion in 11q23 Leading to Fusion of <em>KMT2A</em> With <em>ARHGEF12</em> and Development of B Lineage Acute Lymphoplastic Leukemia in a Child Treated for Acute Myeloid Leukemia Caused by t(9;11)(p21;q23)/<em>KMT2A-MLLT3</em> JF - Cancer Genomics - Proteomics JO - Cancer Genomics Proteomics SP - 67 LP - 81 DO - 10.21873/cgp.20242 VL - 18 IS - 1 AU - IOANNIS PANAGOPOULOS AU - KRISTIN ANDERSEN AU - MARTINE EILERT-OLSEN AU - BERNWARD ZELLER AU - MONICA CHENG MUNTHE-KAAS AU - JOCHEN BUECHNER AU - LIV T.N. OSNES AU - FRANCESCA MICCI AU - SVERRE HEIM Y1 - 2021/01/01 UR - http://cgp.iiarjournals.org/content/18/1/67.abstract N2 - Background/Aim: Fusion of histone-lysine N-methyltransferase 2A gene (KMT2A) with the Rho guanine nucleotide exchange factor 12 gene (ARHGEF12), both located in 11q23, was reported in some leukemic patients. We report a KMT2A-ARHGEF12 fusion occurring during treatment of a pediatric acute myeloid leukemia (AML) with topoisomerase II inhibitors leading to a secondary acute lymphoblastic leukemia (ALL). Materials and Methods: Multiple genetic analyses were performed on bone marrow cells of a girl initially diagnosed with AML. Results: At the time of diagnosis with AML, the t(9;11)(p21;q23)/KMT2A-MLLT3 genetic abnormality was found. After chemotherapy resulting in AML clinical remission, a 2 Mb deletion in 11q23 was found generating a KMT2A-ARHGEF12 fusion gene. When the patient later developed B lineage ALL, a t(14;19)(q32;q13), loss of one chromosome 9, and KMT2A-ARHGEF12 were detected. Conclusion: The patient sequentially developed AML and ALL with three leukemia-specific genomic abnormalities in her bone marrow cells, two of which were KMT2A-rearrangements. ER -