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Similar deficiencies, different outcomes: succinate dehydrogenase loss in adrenal medulla vs. fibroblast cell culture models of paraganglioma.
Cancer Metab
December 2024
Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine and Science, 200 First St. SW, Rochester, MN, 55905, USA.
Heterozygosity for loss-of-function alleles of the genes encoding the four subunits of succinate dehydrogenase (SDHA, SDHB, SDHC, SDHD), as well as the SDHAF2 assembly factor predispose affected individuals to pheochromocytoma and paraganglioma (PPGL), two rare neuroendocrine tumors that arise from neural crest-derived paraganglia. Tumorigenesis results from loss of the remaining functional SDHx gene copy, leading to a cell with no functional SDH and a defective tricarboxylic acid (TCA) cycle. It is believed that the subsequent accumulation of succinate competitively inhibits multiple dioxygenase enzymes that normally suppress hypoxic signaling and demethylate histones and DNA, ultimately leading to increased expression of genes involved in angiogenesis and cell proliferation.
View Article and Find Full Text PDFTET3-facilitated differentiation of human umbilical cord mesenchymal stem cells into oligodendrocyte precursor cells for spinal cord injury recovery.
J Transl Med
December 2024
Department of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, 2075 Qunli Seventh Avenue, Daoli District, Harbin, 150001, Heilongjiang Province, China.
Background: Spinal cord injury (SCI) inflicts a severe burden on patients and lacks effective treatments. Owing to the poor regenerative capabilities of endogenous oligodendrocyte precursor cells (OPCs) following SCI, there is a growing interest in alternative sources, such as human umbilical cord mesenchymal stem cells (HUCMSCs). TET3 is a key DNA demethylase that plays an important role in neural differentiation, but its role in OPC formation is not well understood.
View Article and Find Full Text PDF[Epigenetic reprogramming, germline and genomic imprinting].
Med Sci (Paris)
December 2024
IGMM, Univ Montpellier, CNRS, Montpellier, France.
The memory of cellular identity is crucial for the correct development of an individual and is maintained throughout life by the epigenome. Chromatin marks, such as DNA methylation and histone modifications, ensure the stability of gene expression programmes over time and through cell division. Loss of these marks can lead to severe pathologies, including cancer and developmental syndromes.
View Article and Find Full Text PDFALKBH1: emerging biomarker and therapeutic target for cancer treatment.
Discov Oncol
December 2024
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, USA.
As neoplastic cells proliferate, disseminate, and infiltrate, they undergo substantial alterations in their epigenetic configuration. Among the pivotal enzymes implicated in this phenomenon is the AlkB family of demethylases, notably AlkB homolog 1 (ALKBH1), which demonstrates conspicuous upregulation across various malignancies. The heightened expression of ALKBH1 renders it a compelling candidate for the development of multifaceted anticancer modalities.
View Article and Find Full Text PDFEpigenetic downregulation of the proapoptotic gene in oral squamous cell carcinoma.
Mol Med Rep
March 2025
Department of Biomedical Sciences, National Chung Cheng University, Chia‑Yi 62102, Taiwan, R.O.C.
Homeobox A5 () has been identified as a tumor suppressor gene in breast cancers, but its role in oral squamous cell carcinoma (OSCC) has not been confirmed. The Illumina GoldenGate Assay for methylation identified that DNA methylation patterns differ between tumorous and normal tissues in the oral cavity and that is one of the genes that are hypermethylated in oral tumor tissues. The present study obtained more‑complete information on the methylation status of by using the Illumina Infinium MethylationEPIC BeadChip and bisulfite sequencing assays.
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