ReviewInternational journal of molecular sciences2024
Monocytic Differentiation in Acute Myeloid Leukemia Cells: Diagnostic Criteria, Biological Heterogeneity, Mitochondrial Metabolism, Resistance to and Induction by Targeted Therapies.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Real-world treatment patterns and clinical outcomes in patients with AML from 65 to 74 years unfit for first-line intensive chemotherapy in Japan.International journal of hematology · 2026Article
- Acute Monocytic Leukemia With Histiocyte-Like Morphology and Trisomy 8: A Rare Diagnostic Challenge.Cureus · 2026Article
- Aberrant glycosylation in hematologic malignancies: mechanisms, immune evasion, and therapeutic targeting.Blood cancer journal · 2026Review
- Single-center analysis of relapse risk factors and prognosis in 256 cases of ETV6::RUNX1-positive pediatric acute lymphoblastic leukemia.BMC pediatrics · 2026Article
- Case Report: Acute monocytic leukemia mimicking large-vessel vasculitis onFrontiers in immunology · 2026Article
- Phenazine 5,10-dioxide analogues as potential therapeutics in AML: Efficacy on patient-derived blasts, in zebrafish larvae xenografts and synergy with venetoclax.Translational oncology · 2026Article
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Dual Role of Transformer 2 Beta as Both a Developmental Necessity and a Disease Modulator.International journal of molecular sciences · 2025Review
- Cell Marker Accordion: interpretable single-cell and spatial omics annotation in health and disease.Nature communications · 2025Article
- Ferritin in Acute Myeloid Leukemia: Not Only a Marker of Inflammation and Iron Overload, but Also a Regulator of Cellular Iron Metabolism, Signaling and Communication.International journal of molecular sciences · 2025Review
- Cell Marker Accordion: interpretable single-cell and spatial omics annotation in health and disease.bioRxiv : the preprint server for biology · 2025Article
- Mapping of Functional Metabolic Phenotypes in Acute Myeloid Leukemia.Cancer medicine · 2025Article
- miR-182 promoter hypermethylation predicts the better outcome of AML patients treated with AZA + VEN in a real-world setting.Clinical epigenetics · 2025Article
- XPO1/Exportin-1 in Acute Myelogenous Leukemia; Biology and Therapeutic Targeting.Biomolecules · 2025Review
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Identification of an Ara-C resistance-related gene risk score and the role of S100A4 in AML via NR6A1-dependent activation and p53 regulation.Frontiers in pharmacology · 2025Article
- Heterogeneity of monocytes in cancer.American journal of cancer research · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We review the importance of monocytic differentiation and differentiation induction in non-APL (acute promyelocytic leukemia) variants of acute myeloid leukemia (AML), a malignancy characterized by proliferation of immature myeloid cells. Even though the cellular differentiation block is a fundamental characteristic, the AML cells can show limited signs of differentiation. According to the French-American-British (FAB-M4/M5 subset) and the World Health Organization (WHO) 2016 classifications, monocytic differentiation is characterized by morphological signs and the expression of specific molecular markers involved in cellular communication and adhesion. Furthermore, monocytic FAB-M4/M5 patients are heterogeneous with regards to cytogenetic and molecular genetic abnormalities, and monocytic differentiation does not have any major prognostic impact for these patients when receiving conventional intensive cytotoxic therapy. In contrast, FAB-M4/M5 patients have decreased susceptibility to the Bcl-2 inhibitor venetoclax, and this seems to be due to common molecular characteristics involving mitochondrial regulation of the cellular metabolism and survival, including decreased dependency on Bcl-2 compared to other AML patients. Thus, the susceptibility to Bcl-2 inhibition does not only depend on general resistance/susceptibility mechanisms known from conventional AML therapy but also specific mechanisms involving the molecular target itself or the molecular context of the target. AML cell differentiation status is also associated with susceptibility to other targeted therapies (e.g., CDK2/4/6 and bromodomain inhibition), and differentiation induction seems to be a part of the antileukemic effect for several targeted anti-AML therapies. Differentiation-associated molecular mechanisms may thus become important in the future implementation of targeted therapies in human AML.
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