Myeloperoxidase (MPO) has been associated with both a myeloid lineage commitment and favorable prognosis in patients with acute myeloid leukemia (AML). DNA methyltransferase inhibitors (decitabine and zeburaline) induced MPO gene promoter demethylation and MPO gene transcription in AML cells with low MPO activity. Therefore, MPO gene transcription was directly and indirectly regulated by DNA methylation. A DNA methylation microarray subsequently revealed a distinct methylation pattern in 33 genes, including DNA methyltransferase 3 beta (DNMT3B), in CD34-positive cells obtained from AML patients with a high percentage of MPO-positive blasts. Based on the inverse relationship between the methylation status of DNMT3B and MPO, we found an inverse relationship between DNMT3B and MPO transcription levels in CD34-positive AML cells (P=0.0283). In addition, a distinct methylation pattern was observed in five genes related to myeloid differentiation or therapeutic sensitivity in CD34-positive cells from AML patients with a high percentage of MPO-positive blasts. Taken together, the results of the present study indicate that MPO may serve as an informative marker for identifying a distinct and crucial DNA methylation profile in CD34-positive AML cells.
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http://dx.doi.org/10.1038/leu.2014.15 | DOI Listing |
Curr Rheumatol Rev
January 2025
Department of Rheumatology, Beijing Jishuitan Hospital, Guizhou Hospital, China.
Gouty arthritis is a common arthritic disease caused by the deposition of monosodium urate crystals in the joints and the tissues around it. The main pathogenesis of gout is the inflammation caused by the deposition of monosodium urate crystals. Omics studies help us evaluate global changes in gout during recent years, but most studies used only a single omics approach to illustrate the mechanisms of gout.
View Article and Find Full Text PDFEndocr Metab Immune Disord Drug Targets
January 2025
Department of Laboratory Medicine, Taizhou First People's Hospital, Huangyan Hospital of Wenzhou Medical University, Taizhou, Zhejiang, China.
Aim: The aim of this study is to examine the role of the microrchidia (MORC) family, a group of chromatin remodeling proteins, as the therapeutic and prognostic markers for colorectal cancer (CRC).
Background: MORC protein family genes are a highly conserved nucleoprotein superfamily whose members share a common domain but have distinct biological functions. Previous studies have analyzed the roles of MORCs as epigenetic regulators and chromatin remodulators; however, the involvement of MORCs in the development and pathogenesis of CRC was less examined.
J Pathol
January 2025
Laboratory of Pathology, Center for Cancer Research, NCI, Bethesda, MD, USA.
Rhabdomyosarcoma (RMS) is a family of phenotypically myogenic paediatric cancers consisting of two major subtypes: fusion-positive (FP) RMS, most commonly involving the PAX3::FOXO1 fusion gene, formed by the fusion of paired box 3 (PAX3) and forkhead box O1 (FOXO1) genes, and fusion-negative (FN) RMS, lacking these gene fusions. In humans, DNA methylation patterns distinguish these two subtypes as well as mutation-associated subsets within these subtypes. To investigate the biological factors responsible for these methylation differences, we profiled DNA methylation in RMS tumours derived from genetically engineered mouse models (GEMMs) in which various driver mutations were introduced into different myogenic lineages.
View Article and Find Full Text PDFThe ANZSNP scientific meeting 2024 was held in the scenic city of Queenstown, New Zealand on 31 August and September 1. Dr Fouzia Ziad, President of the ANZSNP and Dr Laveniya Satgunaseelan, Secretary /Treasurer of the ANZSNP were the convenors of the meeting. The meeting was co-badged with the Australasian Winter Conference on Brain Research (AWCBR) 2024.
View Article and Find Full Text PDFNoncoding RNA Res
April 2025
Kresge Eye Institute, Wayne State University, Detroit, MI, USA.
Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc), is also downregulated.
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