确定ZMYM2: FGFR1融合阳性白血病的药物联合策略

Ariane Huang, Sofia R Beer, Christopher A Eide, Brian J Druker, Jeffrey W Tyner, Jessica Leonard, Cristina E Tognon
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引用次数: 0

摘要

嗜酸性粒细胞和酪氨酸激酶基因融合(MLN-TK)的髓/淋巴肿瘤是一类融合蛋白驱动的预后不良的白血病。含有FGFR1融合的白血病以前被称为8p11.2骨髓增生性综合征(EMS)或干细胞白血病/淋巴瘤(SCLL),根据最新的WHO分类系统,目前被称为具有FGFR1重排的髓系/淋巴肿瘤。为了确定MLN-TK患者的新治疗方案,我们评估了一名ZMYM2: fgfr1阳性患者的临床和体外药物反应数据,该患者成功接受了FGFR激酶靶向抑制剂的治疗。在最初对ponatinib有反应后,患者切换到pemigatinib,最终使他们成功移植。从患者身上分离出的白血病细胞对波纳替尼、硼替佐米和阿西替尼表现出体外敏感性。ZMYM2: fgfr1转化的Ba/F3细胞对下一代FGFR抑制剂非常敏感,FGFRi与曲美替尼或米多舒林的组合被发现具有协同作用,为fgfr1融合阳性患者提供了新的治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Identifying Drug Combination Strategies for ZMYM2: FGFR1 Fusion Positive Leukemia.

Myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions (MLN-TK) are a class of fusion protein-driven, poor prognosis leukemias. Leukemias harboring FGFR1 fusions have previously been referred to as 8p11.2 myeloproliferative syndrome (EMS) or stem cell leukemia/lymphoma (SCLL) and are currently referred to as Myeloid/lymphoid neoplasms with FGFR1 rearrangement based on the most recent WHO classification system. To identify new therapeutic options for MLN-TK patients, we evaluated clinical and ex vivo drug response data from a ZMYM2:FGFR1-positive patient who was successfully treated with FGFR kinase-targeting inhibitors. After initially responding to ponatinib, the patient was switched to pemigatinib which eventually transitioned them to a successful transplant. Leukemia cells isolated from the patient exhibited ex vivo sensitivity to ponatinib, bortezomib and axitinib. ZMYM2:FGFR1-transformed Ba/F3 cells were exquisitely sensitive to next generation FGFR inhibitors, and combinations of FGFRi plus trametinib or midostaurin were found to be synergistic, suggesting novel therapeutic options for FGFR1-fusion positive patients.

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