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在急性骨髓性白血病-正常型患者中的基因表达特征和途径分析

Angeli Ambayya^1,2, Rozaimi Razali³, Sarina Sulong⁴

¹Department of Haematology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.

|September 5, 2025

概括

这项研究揭示了正常型急性髓性白血病 (AML-NK) 的关键基因表达差异,确定了潜在治疗点和最小残留疾病监测的途径. 这些发现突显了癌症的特征,并证实了AML-NK病变的转录组失调.

科学领域:

基因组学
分子生物学
癌症学

背景情况:

有正常型的急性髓性白血病 (AML- NK) 呈现显著的异质性,影响治疗结果.
了解AML-NK的分子基础对于改善患者的治疗和生存至关重要.
转录组测序为探索基因表达特征和识别AML-NK中失调的途径提供了强大的工具.

研究的目的:

在马来西亚队列中对AML-NK进行全面的转录组分析.
在诊断和缓解时识别AML-NK的差异表达基因 (DEG) 和失调的途径.
探索已识别的基因和治疗干预和最小残留疾病监测的潜力.

主要方法:

51名AML-NK患者在诊断时进行了转录组测序 (DX),12名患者在第一次缓解 (CR1) 和12名健康对照.
用于差异基因表达分析的定制DESeq2管道.
用基因组丰富分析和RT-qPCR验证来分析途径失调并确认发现.

主要成果:

在AML-NK和健康对照组中发现了5126个DEG,其中85. 8%是编码基因.
在AML-NK DX和CR1样本中发现了5,621个DEG,影响了20个路径类别.
增殖途径 (细胞循环,DNA复制) 被上调,而与免疫相关的途径被下调. 在DX与CR1研究中发现瘤基因过度表达 (FLT3,MYB,DNMT3B,MYCN).

结论:

在AML-NK发病过程中验证了转录基因失调,重现了癌症的特征.
已识别的DEG和通路为AML-NK分子机制提供了洞察力.
过度表达的瘤基因是AML-NK中最小残留疾病监测的潜在标志物.

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