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| http://dx.doi.org/10.3343/alm.2015.35.2.260 | DOI Listing |
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A distinct subgroup of AML resembling the APL immunophenotype is associated with DIC.
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December 2024
Department of Hematology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Article Synopsis
- This study identified a subgroup of acute myeloid leukemia (AML) patients with an APL-like immunophenotype characterized by the absence of CD34 and HLA-DR, aiming to explore differences in clinical and molecular features between them and regular AML patients.
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Division of Hematology/Medical Oncology, Department of Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Leukaemia stem cells (LSCs) are major contributors to chemoresistance in acute myeloid leukaemia (AML). Identifying potential biomarkers within LSCs that can predict chemosensitivity in AML is key. This prospective study involved 20 consecutive de novo AML patients who underwent '7 + 3' induction therapy.
View Article and Find Full Text PDFRSK1 dependency in FLT3-ITD acute myeloid leukemia.
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Division of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Internal tandem duplications (ITD) in fms-like tyrosine kinase 3 (FLT3) represent the most common genetic alteration in de novo acute myeloid leukemia (AML). Here, we identify ribosomal protein s6 kinase a1 (RSK1) as a core dependency in FLT3-ITD AML and unveil the existence of crucial bi-directional regulation. RSK1 perturbation resulted in marked apoptosis and abrogated phosphorylation of FLT3 and associated downstream signaling cascades in FLT3-ITD AML cell lines.
View Article and Find Full Text PDFAn updated outlook on autophagy mechanism and how it supports acute myeloid leukemia maintenance.
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View Article and Find Full Text PDFNAT10-mediated mRNA N-acetylcytidine reprograms serine metabolism to drive leukaemogenesis and stemness in acute myeloid leukaemia.
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State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
RNA modification has emerged as an important epigenetic mechanism that controls abnormal metabolism and growth in acute myeloid leukaemia (AML). However, the roles of RNA N-acetylcytidine (ac4C) modification in AML remain elusive. Here, we report that ac4C and its catalytic enzyme NAT10 drive leukaemogenesis and sustain self-renewal of leukaemic stem cells/leukaemia-initiating cells through reprogramming serine metabolism.
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