Therapy-induced Deletion in 11q23 Leading to Fusion of KMT2A With ARHGEF12 and Development of B Lineage Acute Lymphoplastic Leukemia in a Child Treated for Acute Myeloid Leukemia Caused by t(9;11)(p21;q23)/KMT2A-MLLT3.,Cancer Genomics & Proteomics

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Therapy-induced Deletion in 11q23 Leading to Fusion of KMT2A With ARHGEF12 and Development of B Lineage Acute Lymphoplastic Leukemia in a Child Treated for Acute Myeloid Leukemia Caused by t(9;11)(p21;q23)/KMT2A-MLLT3.
Cancer Genomics & Proteomics ( IF 2.6 ) Pub Date : 2021-01-08 , DOI: 10.21873/cgp.20242
Ioannis Panagopoulos ₁ , Kristin Andersen ₂ , Martine Eilert-Olsen ₂ , Bernward Zeller ₃ , Monica Cheng Munthe-Kaas ₃ , Jochen Buechner ₃ , Liv T N Osnes ₄ , Francesca Micci ₂ , Sverre Heim _{2,

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Affiliation

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).

中文翻译：

治疗诱导的 11q23 缺失导致 KMT2A 与 ARHGEF12 融合和 B 系急性淋巴细胞白血病的发展，该儿童接受了由 t(9;11)(p21;q23)/KMT2A-MLLT3 引起的急性髓细胞白血病治疗。

在一些白血病患者中报道了组蛋白-赖氨酸 N-甲基转移酶 2A 基因 (KMT2A) 与 Rho 鸟嘌呤核苷酸交换因子 12 基因 (ARHGEF12) 的融合，两者均位于 11q23。我们报告了在使用拓扑异构酶 II 抑制剂治疗小儿急性髓性白血病 (AML) 期间发生的 KMT2A-ARHGEF12 融合，导致继发性急性淋巴细胞白血病 (ALL)。

更新日期：2021-01-11

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