当前位置: X-MOL 学术Cancer Genom. Proteom. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
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, 5
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
down
wechat
bug