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    Editorial: Acute leukemias: molecular characterization, leukemia-initiating cells, and influence of the microenvironment, volume II
    (Frontiers, 06.01.2025) Varışli, Lokman; Dancik, Garrett M.; Copland, John A.; Vlahopoulos, Spiros A.
    Acute leukemia is a wide group of hematologic malignancies that arise from leukemiainitiating cells (LICs), also known as leukemic stem cells (LSCs), which originate from transformed hematopoietic stem cells (HSCs) in the bone marrow. Leukemic cells accumulate various genetic and epigenetic defects, both inherited from the LICs they originate from and acquired later. Genetic defects in leukemic cells determine their biological behavior and, as expected, affect the prognosis of the disease and its response to treatment. Therefore, molecular characterization of the disease is important for all stages of the disease, such as predicting prognosis, determining the treatment approach, and evaluating the possibility of recurrence. In this context, a better understanding of the molecular mechanisms of acute leukemia will enable the emergence of simpler and more effective treatment approaches and increase the rate of treated patients.
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    Investigating the biology of microRNA links to ALDH1A1 reveals candidates for preclinical testing in acute myeloid leukemia
    (Spandidos Publications, 30.10.2024) Vlahopoulos, Spiros A.; Varışli, Lokman; Zoumpourlis, Panagiotis; Spandidos, Demetrios A.; Zoumpourlis, Vassilis
    Aldehyde dehydrogenase 1 family member A1 (ALDH1A1) is a member of the aldehyde dehydrogenase gene subfamily that encode enzymes with the ability to oxidize retinaldehyde. It was recently shown that high ALDH1A1 RNA abundance correlates with a poor prognosis in acute myeloid leukemia (AML). AML is a hematopoietic malignancy associated with high morbidity and mortality rates. Although there are a number of agents that inhibit ALDH activity, it would be crucial to develop methodologies for adjustable genetic interference, which would permit interventions on several oncogenic pathways in parallel. Intervention in multiple oncogenic pathways is theoretically possible with microRNAs (miRNAs or miRs), a class of small non‑coding RNAs that have emerged as key regulators of gene expression in AML. A number of miRNAs have shown the ability to interfere with ALDH1A1 gene expression directly in solid tumor cells, and these miRNAs can be evaluated in AML model systems. There are indications that a few of these miRNAs actually do have an association with AML disease course, rendering them a promising target for genetic intervention in AML cells.
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    The Molecular context of oxidant stress response in cancer establishes ALDH1A1 as a critical target: What this means for acute myeloid leukemia
    (MDPI, 2023) Dancik, Garrett M.; Varışli, Lokman; Vlahopoulos, Spiros A.
    The protein family of aldehyde dehydrogenases (ALDH) encompasses nineteen members. The ALDH1 subfamily consists of enzymes with similar activity, having the capacity to neutralize lipid peroxidation products and to generate retinoic acid; however, only ALDH1A1 emerges as a significant risk factor in acute myeloid leukemia. Not only is the gene ALDH1A1 on average significantly overexpressed in the poor prognosis group at the RNA level, but its protein product, ALDH1A1 protects acute myeloid leukemia cells from lipid peroxidation byproducts. This capacity to protect cells can be ascribed to the stability of the enzyme under conditions of oxidant stress. The capacity to protect cells is evident both in vitro, as well as in mouse xenografts of those cells, shielding cells effectively from a number of potent antineoplastic agents. However, the role of ALDH1A1 in acute myeloid leukemia has been unclear in the past due to evidence that normal cells often have higher aldehyde dehydrogenase activity than leukemic cells. This being true, ALDH1A1 RNA expression is significantly associated with poor prognosis. It is hence imperative that ALDH1A1 is methodically targeted, particularly for the acute myeloid leukemia patients of the poor prognosis risk group that overexpress ALDH1A1 RNA.