Abstract

In this post-genomic era, long noncoding RNAs (lncRNAs) are rapidly gaining recognition for their crucial roles across diverse biological processes and contexts. The human blood system is no exception, where dozens of lncRNAs have been established as regulators of normal and/or malignant hematopoiesis, and where ongoing works continue to uncover novel lncRNA functions. Our review focuses on lncRNAs that are involved in the pathogenesis of acute myeloid leukemia (AML) and the mechanisms through which they control gene expression in this disease context. We also comment on genome-wide sequencing or profiling studies that have implicated large sets of lncRNAs in AML pathophysiology.

Highlights

  • ON long noncoding RNA (lncRNA) AND acute myeloid leukemia (AML)Hematopoietic stem cell (HSC) homeostasis and lifelong blood formation rely on a complex interplay between many different pathways

  • Our review focuses on lncRNAs that are involved in the pathogenesis of acute myeloid leukemia (AML) and the mechanisms through which they control gene expression in this disease context

  • Based solely on lncRNA expression, the authors distinguished four molecular subtypes that differ in prognoses and active pathways and that behave independently of the European Leukemia Net (ELN) risk classification groups. These lncRNA-based subgroups lacked high concordance with conventional clinical or genetic factors, there was, some association with traditional molecular determinants such as mutations in CEBPA, NPM1, TP53, and FLT3-ITD [40]. Another recent study of cytogenetically normal (CN)-AML cases with leukemia stem cell (LSC)-associated core-enriched gene expression signatures (CE-GES) discovered a set of 111 lncRNAs that strongly correlate with the LSC signature [41]

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Summary

Introduction

ON lncRNAs AND AMLHematopoietic stem cell (HSC) homeostasis and lifelong blood formation rely on a complex interplay between many different pathways. Our review focuses on lncRNAs that are involved in the pathogenesis of acute myeloid leukemia (AML) and the mechanisms through which they control gene expression in this disease context. Another recent study of CN-AML cases with leukemia stem cell (LSC)-associated core-enriched gene expression signatures (CE-GES) discovered a set of 111 lncRNAs that strongly correlate with the LSC signature [41].

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