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The role of lnc‑MAPKAPK5‑AS1 in immune cell infiltration in hepatocellular carcinoma: Bioinformatics analysis and validation.
Oncol Lett
March 2025
Guangzhou Center for Disease Control and Prevention, School of Public Health, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
The oncogenic and tumor suppressor roles of lnc-MAPKAPK5-AS1 in multiple cancers suggest its complexity in modulating cancer progression. The expression and promoter methylation level of lnc-MAPKAPK5-AS1 in hepatocellular carcinoma (HCC) was investigated through data mining from The Cancer Genome Atlas and Gene Expression Omnibus and its significance in prognosis and immunity was explored. lnc-MAPKAPK5-AS1 was co-expressed with its protein-coding gene MAPKAPK5 in HCC and exhibited upregulation in HCC tissues as a result of hypomethylation of its promoter region.
View Article and Find Full Text PDFSomatic mutations and DNA methylation identify a subgroup of poor prognosis within lower-risk myelodysplastic syndromes.
Hemasphere
January 2025
Université Paris Cité, Institut Cochin, INSERM U1016, CNRS UMR8104 Assistance Publique-Hôpitaux de Paris.Centre, Laboratory of Hematology, Hôpital Cochin Paris France.
Lower risk (LR) myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem and progenitor disorders caused by the accumulation of somatic mutations in various genes including epigenetic regulators that may produce convergent DNA methylation patterns driving specific gene expression profiles. The integration of genomic, epigenomic, and transcriptomic profiling has the potential to spotlight distinct LR-MDS categories on the basis of pathophysiological mechanisms. We performed a comprehensive study of somatic mutations and DNA methylation in a large and clinically well-annotated cohort of treatment-naive patients with LR-MDS at diagnosis from the EUMDS registry (ClinicalTrials.
View Article and Find Full Text PDFAdvanced Distance-Resolved Evaluation of the Perienhancing Tumor Areas with FLAIR Hyperintensity Indicates Different ADC Profiles by Promoter Methylation Status in Glioblastoma.
AJNR Am J Neuroradiol
January 2025
From the Department of Neuroradiology (G.B., N.H., F.D.v.D., A.B., Z.K.), University Hospital Zürich, Zürich, Switzerland.
Background And Purpose: Whether differences in the O-methylguanine-DNA methyltransferase () promoter methylation status of glioblastoma (GBM) are reflected in MRI markers remains largely unknown. In this work, we analyze the ADC in the perienhancing infiltration zone of GBM according to the corresponding status by using a novel distance-resolved 3D evaluation.
Materials And Methods: One hundred one patients with wild-type GBM were retrospectively analyzed.
MGST1 overexpression ameliorates mitochondrial dysfunction and ferroptosis during myocardial ischemia/reperfusion injury after heart transplantation.
Int J Biol Macromol
January 2025
Department of Thoracic Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Electronic address:
Mitochondrial dysfunction and ferroptosis play crucial roles in myocardial ischemia/reperfusion (I/R) following heart transplantation. Microsomal glutathione s transferase 1 (MGST1) is widely distributed in mitochondria and has a protective effect against ferroptosis, and its involvement in myocardial I/R injury has not yet been elucidated. In this study, donor hearts from C57BL/6 male mice were subjected to 12 h of ex-vivo cold ischemia treatment and transplanted into the abdomen of recipient mice for 24 h of reperfusion.
View Article and Find Full Text PDFAberrant DNA methylation of EDNRB, MGMT and TIMP3 gene promoters in saliva of head and neck carcinoma patients as a diagnostic tool.
Mol Biol Rep
January 2025
Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Background: Differential DNA methylation in the promoter region of tumour suppressor genes leads to gene function silencing.
Materials And Methods: In this study, we aimed to evaluate the salivary promoter methylation of EDNRB, MGMT and TIMP3 genes in H&NC patients (n = 100), premalignant lesions patients (n = 25) and healthy controls (n = 50). Blood and saliva samples were collected from all three groups and 20 concomitant tumour tissues were collected from the H&NC patients.
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