Blood Res (2024) 59:39

Published online December 2, 2024

https://doi.org/10.1007/s44313-024-00041-7

© The Korean Society of Hematology

How to improve AML outcomes?

Taner Tan1 and Sinem Civriz Bozdag1*

1 Department of Hematology, ͣKoc University Medical School, Istanbul, Turkey

Correspondence to : *Sinem Civriz Bozdag
scivriz@hotmail.com; sbozdag@kuh.ku.edu.tr

Received: June 5, 2024; Accepted: August 25, 2024

© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

Abstract

Understanding the intricacies of the pathophysiology and genomic landscape has enhanced the long-term outcomes for patients with acute myeloid leukemia (AML). The identification of novel molecular targets has introduced new therapeutic strategies that attempt to surpass the dominance of the "7 + 3 regimen" established in the 1970s. In 2022, the World Health Organization and International Consensus Classification revised their definitions and approaches to AML, reflecting the current and evolving changes at the molecular level. The guidelines are now grounded in a definition of the disease that emphasizes genetic characteristics. Today, we recognize AML as a genetically diverse disease; a retrospective study identified 5234 driver mutations across 76 genes or genomic regions, with two or more drivers observed in 86% of patients (Papaemmanuil et al., N Engl J Med 374:2209–21, 2016).

Keywords AML, Treatment, Relapsed, Targeted, Mutations, Outcome

Article

REVIEW

Blood Res 2024; 59():

Published online December 2, 2024 https://doi.org/10.1007/s44313-024-00041-7

Copyright © The Korean Society of Hematology.

How to improve AML outcomes?

Taner Tan1 and Sinem Civriz Bozdag1*

1 Department of Hematology, ͣKoc University Medical School, Istanbul, Turkey

Correspondence to:*Sinem Civriz Bozdag
scivriz@hotmail.com; sbozdag@kuh.ku.edu.tr

Received: June 5, 2024; Accepted: August 25, 2024

© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

Abstract

Understanding the intricacies of the pathophysiology and genomic landscape has enhanced the long-term outcomes for patients with acute myeloid leukemia (AML). The identification of novel molecular targets has introduced new therapeutic strategies that attempt to surpass the dominance of the "7 + 3 regimen" established in the 1970s. In 2022, the World Health Organization and International Consensus Classification revised their definitions and approaches to AML, reflecting the current and evolving changes at the molecular level. The guidelines are now grounded in a definition of the disease that emphasizes genetic characteristics. Today, we recognize AML as a genetically diverse disease; a retrospective study identified 5234 driver mutations across 76 genes or genomic regions, with two or more drivers observed in 86% of patients (Papaemmanuil et al., N Engl J Med 374:2209–21, 2016).

Keywords: AML, Treatment, Relapsed, Targeted, Mutations, Outcome

Fig 1.

Figure 1.Hierarchical classification of the International Consensus Classification of AML. AML—Acute Myeloid Leukemia, ASXL1—Additional Sex Combs Like 1, BCOR—BCL6 Corepressor, EZH2—Enhancer of Zeste Homolog 2, MDS—Myelodysplastic Syndrome, MPN—Myeloproliferative Neoplasm, RUNX1—Runt-Related Transcription Factor 1, SF3B1—Splicing Factor 3b Subunit 1, SRSF2—Serine/Arginine-Rich Splicing Factor 2, STAG2—Stromal Antigen 2, TP53—Tumor Protein 53, U2AF1—U2 Small Nuclear RNA Auxiliary Factor 1, VAF—Variant Allele Frequency, ZRSR2—Zinc Finger CCCH-Type, RNA-Binding Motif and Serine/Arginine-Rich 2

Fig 2.

Figure 2.2022 ELN risk classification by genetics at initial diagnosis. AML—Acute Myeloid Leukemia, ASXL1—Additional Sex Combs Like 1, BCOR—BCL6 Corepressor, CEBPA—CCAAT Enhancer Binding Protein Alpha, CREBBP—CREB Binding Protein, EZH2—Enhancer of Zeste Homolog 2, FLT3-ITD—FMS-like Tyrosine Kinase 3-Internal Tandem Duplication, GATA2—GATA Binding Protein 2, KMT2A—Lysine Methyltransferase 2A, MEF2C—Myocyte Enhancer Factor 2C, MLLT3—Myeloid/Lymphoid or Mixed-Lineage Leukemia Translocated to 3, MYH11—Myosin Heavy Chain 11, NPM1—Nucleophosmin 1, NUP214—Nucleoporin 214, RUNX1—Runt-Related Transcription Factor 1, SF3B1—Splicing Factor 3b Subunit 1, SRSF2—Serine/Arginine-Rich Splicing Factor 2, STAG2—Stromal Antigen 2, TP53—Tumor Protein 53, U2AF1—U2 Small Nuclear RNA Auxiliary Factor 1, ZRSR2—Zinc Finger CCCH-Type, RNA-Binding Motif and Serine/Arginine-Rich 2

Fig 3.

Figure 3.a b Treatment Algorithm for Newly diagnosed patients with AML fit for intensive therapy. AML—Acute Myeloid Leukemia, CBF—Core Binding Factor, CK—Complex Karyotype, CPX351—Liposomal Daunorubicin and Cytarabine, FLT3—FMS-like Tyrosine Kinase 3, GO—Gemtuzumab Ozogamicin, HMA—Hypomethylating Agents, tAML—Therapy-Related Acute Myeloid Leukemia, AML-MR—Acute Myeloid Leukemia with Myelodysplasia-Related Changes, TP53—Tumor Protein 53, Ven—Venetoclax
Blood Res
Volume 60 2025

Stats or Metrics

Share this article on

  • line

Related articles in BR

Blood Research

pISSN 2287-979X
eISSN 2288-0011
qr-code Download