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Many Roads Lead to snoRNAs

The Ever-Expanding Universe of Non-Coding RNAs in Acute Myeloid Leukemia

Fröhling, Stefan

doi: 10.1097/HS9.0000000000000014
HemaTopics
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National Center for Tumor Diseases Heidelberg, German Cancer Research Center, Heidelberg University Hospital, Heidelberg, Germany

Correspondence: Stefan Fröhling, National Center for Tumor Diseases Heidelberg, German Cancer Research Center, Heidelberg University Hospital, Heidelberg, Germany.

The authors has indicated they have no potential conflicts of interest to disclose.

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

While chimeric fusion genes resulting from balanced chromosomal translocations have long been recognized as “drivers” of acute myeloid leukemia (AML), their critical downstream mediators are incompletely understood. In particular, common effector programs that are shared by various leukemogenic fusion genes, and may thus represent attractive targets for therapeutic intervention, remain elusive. Carsten Müller-Tidow and colleagues now demonstrate that fusion oncoproteins such as RUNX1T1-RUNX1 (also known as AML1-ETO) and MLLT3-KMT2A (also known as MLL-AF9) contribute to AML development by upregulating the expression of a distinct subset of small nucleolar RNAs (snoRNAs) that promote leukemogenesis via enhanced formation of snoRNA ribonucleoprotein complexes, induction of rRNA methylation, increased protein translation, and possibly other mechanisms. This first investigation into the functional consequences of aberrant snoRNA expression in AML adds to the ever-expanding catalog of non-coding RNAs involved in myeloid leukemogenesis, and raises the intriguing possibility that snoRNA deregulation may be a unifying feature of this disease. Furthermore, these data provide a starting point for future studies of the mechanistic link(s) between different types of leukemogenic driver mutations and snoRNA expression and the potential of snoRNAs as tractable therapeutic targets.

Link to: Zhou et al. Nat Cell Biol. 2017;19(7):844–855. PMID: 28650479; https://www.nature.com/articles/ncb3563

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Copyright © 2017 The Authors. Published by Wolters Kluwer Health Inc., on behalf of the European Hematology Association.