Acute Myeloid Leukemia with t(6;9)(p23;q34.1); DEK-NUP214: The Pathogenesis and Potential.

Juli-Anne Gardner, Liam Donnelly, Rebecca Goetz, Brianna Waller, Katherine Devitt
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Abstract

Objectives: Acute myeloid leukemia (AML) is caused by the arrested differentiation and dysregulated proliferation of myeloid precursors. Many AMLs harbor genetic abnormalities which determine the molecular mechanisms of the disease and are associated with distinct clinical and pathological features, prognosis, and targeted therapies. We present a case of acute myeloid leukemia with t(6;9)(p23;q34.1) and review the classic clinical presentations and underlying pathogenesis of the disease.

急性髓系白血病伴t(6;9)(p23;q34.1);DEK-NUP214:发病机制和潜力。
目的:急性髓细胞白血病(AML)是由髓细胞前体分化受阻和增殖失调引起的。许多aml含有遗传异常,这决定了疾病的分子机制,并与独特的临床和病理特征、预后和靶向治疗相关。我们报告一例急性髓性白血病伴t(6;9)(p23;q34.1),并回顾该疾病的经典临床表现和潜在发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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