Targeting Hallmarks of Acute Myelocytic Leukemia (AML): Differentiation Induction in Non-Acute Promyelocytic Leukemia (Non-APL) AML
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".
Deadline for manuscript submissions: 31 July 2026 | Viewed by 4139
Editor
Interests: cancer biology; anakoinosis; oncology; hematological malignancies
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Special Issue Information
Dear Colleagues,
Clinical trials have revealed that the potential for inducing differentiation is present in non-acute promyelocytic leukemia (non-APL) acute myeloid leukemia (AML), even in cases with complex, abnormal phenotypes. Promoting differentiation as a therapeutic option is valuable, as AML often arises in elderly patients who have a reduced chance of being cured by systemic therapy, which often compromises quality of life. The successful introduction of targeted therapies in AML subgroups is promising.
In practice, many questions remain regarding the most effective method of inducing apoptosis in AML via differentiation, given the significant heterogeneity of acquired chromosomal aberrations in this type of acute leukemia.
The differentiation trajectories induced by ATRA are the most well-studied and reveal a gene regulatory circuit that could be widely applied to induce differentiation in AML. However, ATRA monotherapy leads to insufficient clinical results in non-APL AML. Nevertheless, targeting hallmarks of AML opens up the possibility of diversifying therapeutic trajectories by the feasibility of their targeted reprogramming.
To extend the possibilities of phenotypic unlocking AML, potential non-oncogene-addicted (NOA) targets must be considered as circuits that are tightly regulated by acquired oncogenic events via the AML transcriptional landscape. Therefore, reprogramming the oncogene-triggered transcription via epigenetic modifiers and targeted therapies that aim to target specific NOAs facilitate the reversion of oncogene-driven AML phenotypes. An even more comprehensive approach is the combined targeting of receptor-triggered transcription factors with respective agonists/antagonists for reprogramming NOA networks in AML hallmarks and/or stress responses. Such approaches have been shown to induce complete remission in relapsed/refractory AML at a low rate of toxicity, even in an outpatient setting, and could form the basis for subsequent curative immunotherapy.
We are pleased to invite you to contribute to a Special Issue that welcomes original clinical and pre-clinical research, review articles and case reports on the induction of differentiation in non-APL AML, as well as more comprehensive studies on the phenotypic unlocking of AML hallmarks.
Prof. Dr. Albrecht Reichle
Guest Editor
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Keywords
- differentiation induction in non-APL AML
- phenotypic unlocking of AML hallmarks
- targeting non-oncogene addictions in AML
- small molecules with differentiation-inducing capacity
- epigenetic modelling in AML (azacitidine, decitabine)
- receptor-triggered transcription factors in AML
- combined targeting of receptor-triggered transcription factors in AML
- metronomic application of AML therapy
- reduction in treatment toxicity by phenotypic unlocking of AML hallmarks
- combination therapies for phenotypic unlocking of AML hallmarks
- acquired genetic/molecular-genetic aberrations and adaptation of differentiation promoting therapy in AML
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