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ALKBH3-mediated m1A demethylation promotes the malignant progression of acute myeloid leukemia by regulating ferroptosis through the upregulation of ATF4 expression.
Hematology
December 2025
The Basic Medical Laboratory of the 920th Hospital of Joint Logistics Support Force of PLA, The Transfer Medicine Key Laboratory of Cell Therapy Technology of Yunan Province, The Integrated Engineering Laboratory of Cell Biological Medicine of State and Regions, Kunming, Yunnan Province, People's Republic of China.
To investigate the role of ALKBH3 in acute myeloid leukemia (AML), we constructed an animal model of xenotransplantation of AML. Our study demonstrated that ALKBH3-mediated m1A demethylation inhibits ferroptosis in KG-1 cells by increasing ATF4 expression, thus promoting the development of AML. These findings suggest that reducing ALKBH3 expression may be a potential strategy to mitigate AML progression.
View Article and Find Full Text PDFSafety and infection risk factors in elderly acute myeloid leukemia patients undergoing induction therapy with venetoclax combined with hypomethylating agents.
Am J Cancer Res
December 2024
Department of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China Hefei 230001, Anhui, China.
Objective: To retrospectively analyze the incidence of infections in elderly acute myeloid leukemia (AML) patients undergoing induction therapy with venetoclax combined with hypomethylating agents and to compare these findings with those from patients receiving standard or low-dose chemotherapy.
Methods: Medical records of 169 elderly (≥60 years old) AML patients diagnosed via MICM (morphology, immunology, cytogenetics, and molecular genetics) at the First Affiliated Hospital of USTC between June 2019 and June 2022 were reviewed. Patients were divided into three groups: venetoclax combined with hypomethylating agents group (targeted therapy group), standard chemotherapy group, and low-dose chemotherapy group.
Unlabelled: is one of the three most frequently mutated genes in age-related clonal hematopoiesis (CH), alongside and . CH can progress to myeloid malignancies including chronic monomyelocytic leukemia (CMML), and is also strongly associated with inflammatory cardiovascular disease and all-cause mortality in humans. DNMT3A and TET2 regulate DNA methylation and demethylation pathways respectively, and loss-of-function mutations in these genes reduce DNA methylation in heterochromatin, allowing de-repression of silenced elements in heterochromatin.
View Article and Find Full Text PDFInversion of chromosome 16 [inv(16)] is one of the most common chromosomal rearrangements in Acute Myeloid Leukemia (AML) and generates the fusion gene , which initiates leukemogenesis. Patients with inv(16) at diagnosis invariably have the rearrangement at relapse, leading to the assumption that is required after leukemic transformation. However, this has yet to be shown experimentally.
View Article and Find Full Text PDFAcute myeloid leukemias (AMLs) have an overall poor prognosis with many high-risk cases co-opting stem cell gene regulatory programs, yet the mechanisms through which this occurs remain poorly understood. Increased expression of the stem cell transcription factor, MECOM, underlies one key driver mechanism in largely incurable AMLs. How MECOM results in such aggressive AML phenotypes remains unknown.
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