Emerging Agents and Regimens for AML

Overview

Journal J Hematol Oncol

Publisher Biomed Central

Specialties Hematology
Oncology

Date 2021 Mar 24

PMID 33757574

Citations 94

Authors

Hongtao Liu

Affiliations

Soon will be listed here.

Abstract

Until recently, acute myeloid leukemia (AML) patients used to have limited treatment options, depending solely on cytarabine + anthracycline (7 + 3) intensive chemotherapy and hypomethylating agents. Allogeneic stem cell transplantation (Allo-SCT) played an important role to improve the survival of eligible AML patients in the past several decades. The exploration of the genomic and molecular landscape of AML, identification of mutations associated with the pathogenesis of AML, and the understanding of the mechanisms of resistance to treatment from excellent translational research helped to expand the treatment options of AML quickly in the past few years, resulting in noteworthy breakthroughs and FDA approvals of new therapeutic treatments in AML patients. Targeted therapies and combinations of different classes of therapeutic agents to overcome treatment resistance further expanded the treatment options and improved survival. Immunotherapy, including antibody-based treatment, inhibition of immune negative regulators, and possible CAR T cells might further expand the therapeutic armamentarium for AML. This review is intended to summarize the recent developments in the treatment of AML.

Citing Articles

Leukemia-Derived Dendritic Cells Induce Anti-Leukemic Effects Ex Vivo in AML Independently of Patients' Clinical and Biological Features.

Klauer L, Rejeski H, Ugur S, Rackl E, Abdulmajid J, Fischer Z Int J Mol Sci. 2025; 26(4).

PMID: 40004163 PMC: 11855365. DOI: 10.3390/ijms26041700.

Systematic review and meta-analysis of the impact of abnormal expression of long non coding RNA on the prognosis of acute myeloid leukemia.

Liu G, Sun L, Lv P, Qiao R, Wang L, Jin A Front Genet. 2025; 16:1524449.

PMID: 39967688 PMC: 11832533. DOI: 10.3389/fgene.2025.1524449.

Unveiling the potential of CLL-1: a promising target for AML therapy.

Soleimani Samarkhazan H, Zehtabcheh S, Seraji H, Beqaj S, Tayefeh S, Mohammadi M Biomark Res. 2025; 13(1):28.

PMID: 39940055 PMC: 11823018. DOI: 10.1186/s40364-025-00738-6.

Src inhibition potentiates MCL-1 antagonist activity in acute myeloid leukemia.

Hu X, Li L, Nkwocha J, Kmieciak M, Shang S, Cowart L Signal Transduct Target Ther. 2025; 10(1):50.

PMID: 39924517 PMC: 11808118. DOI: 10.1038/s41392-025-02125-x.

Caspase 3-specific cleavage of ubiquitin-specific peptidase 48 enhances drug-induced apoptosis in AML.

Zhang Z, Lin X, Yang Y, Wang X, Wang Y, Huang X Cancer Biol Ther. 2025; 26(1):2459426.

PMID: 39878157 PMC: 11781246. DOI: 10.1080/15384047.2025.2459426.

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