关键词: RARA::STAT5b STAT3::RARA acute promyelocytic leukemia variant acute promyelocytic leukemia

Mesh : Humans Leukemia, Promyelocytic, Acute / drug therapy genetics Tretinoin STAT3 Transcription Factor / genetics

来  源:   DOI:10.1002/mc.23672

Abstract:
Acute promyelocytic leukemia (APL) with typically PML::RARA fusion gene caused by t (15;17) (q22; q12) was distinguished from other types of acute myeloid leukemia. In a subset of patients with APL, t (15;17) (q22;q21) and PML::RARA fusion cannot be detected. In this report, we identified the coexistence of STAT3::RARA and RARA::STAT5b fusions for the first time in a variant APL patient lacking t (15;17)(q22;q21)/PML::RARA fusion. Then, this patient was resistant to all-trans retinoic acid combined arsenic trioxide chemotherapy. Accurate detection of RARA gene partners is crucial for variant APL, and effective therapeutic regime is urgently needed.
摘要:
由t(15;17)(q22;q12)引起的通常具有PML::RARA融合基因的急性早幼粒细胞白血病(APL)与其他类型的急性髓细胞性白血病不同。在一部分APL患者中,t(15;17)(q22;q21)和PML::RARA融合不能被检测到。在这份报告中,我们首次在缺乏t(15;17)(q22;q21)/PML::RARA融合的变异APL患者中发现STAT3::RARA和RARA::STAT5b融合共存.然后,该患者对全反式维甲酸联合三氧化二砷化疗耐药.准确检测RARA基因伴侣对于变异APL至关重要,迫切需要有效的治疗方案。
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