Lineage switch of B‐acute lymphoblastic leukemia with t(11;19)(q23;p13.3) into acute myeloid leukemia with monocytic differentiation after induction chemotherapy

A 65-year old woman with dyspnea, headaches, and epistaxis presented anemia (hemoglobin 7.7 g/dL) thrombocytopenia (platelets 18×109/L) a white blood cell (WBC) count of 4.0 × 109/L 60% circulating blasts. Bone marrow blast percentage was 95%, blasts were small to intermediate in size reticulated chromatin scant cytoplasm on bone aspirate (Figure 1, panel A, original magnification 1000×, Wright–Giemsa stain) biopsy B, 600×, hematoxylin eosin stain). The leukemic cells had B (CD19+CD20−CD22+cCD79a+) immunophenotype without markers immaturity (CD34−Tdt− CD10−) or myeloid lineage (MPO−CD33−CD13−, Figure C). Cytogenetic study showed t(11;19)(q23;p13.3) D), fluorescence situ hybridization confirmed KMT2A::MLLT1 fusion (nuc ish(MLL,MLLT1)x3(MLL con MLLT1×2)[479/500]). After one cycle hyper-CVAD chemotherapy, she remained anemic 7.6 improved 169 109/L) WBC 2.1 109/L. subsequent E, F, acute leukemia monocytic differentiation 71% monoblasts promonocytes. Leukemic expressed CD33 lysozyme variable retained PAX5 G, 200×). karyotype persistent disease switch. patient then received Venetoclax combined FLAG-IDA (fludarabine, cytarabine, idarubicin, granulocyte colony-stimulating factor) induction, achieved complete remission. next step the treatment plan will be matched, unrelated donor allogeneic stem transplant. Lineage switch leukemia, including B-ALL t(11;19)(q23;p13.3), has been reported pediatric patients (PMID: 22685031; 35409391) but is rare adult patients, often occurs after even during induction confers poor prognosis. Most such harbor MLL (KMT2A) gene rearrangements. authors have nothing report. declare no conflict interest.