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| http://dx.doi.org/10.1038/oncsis.2015.4 | DOI Listing |
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Association of Germline Pathogenic Variants in and Other DNA Damage Response Genes With Lung Cancer Risk Among Non-Hispanic Whites and African Americans.
JCO Precis Oncol
January 2025
Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, MI.
Purpose: Although lung cancer is one of the most common malignancies, the underlying genetics regarding susceptibility remain poorly understood. We characterized the spectrum of pathogenic/likely pathogenic (P/LP) germline variants within DNA damage response (DDR) genes among lung cancer cases and controls in non-Hispanic Whites (NHWs) and African Americans (AAs).
Materials And Methods: Rare, germline variants in 67 DDR genes with evidence of pathogenicity were identified using the ClinVar database.
Telomeres are hypersensitive to the formation of the common oxidative lesion 8-oxoguanine (8oxoG), which impacts telomere stability and function. OGG1 and MUTYH glycosylases initiate base excision repair (BER) to remove 8oxoG or prevent mutation. Here, we show OGG1 loss or inhibition, or MUTYH loss, partially rescues telomeric 8oxoG-induced premature senescence and associated proinflammatory responses, while loss of both glycosylases causes a near complete rescue in human fibroblasts.
View Article and Find Full Text PDFRole of Mutyh in Oxidative Stress Damage in Retinopathy of Prematurity.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
December 2024
Department of Neonatology, Children's Hospital of Nanjing Medical University,Nanjing 210000,China.
Objective To explore the role of the base mismatch repair gene Mutyh in retinopathy of prematurity(ROP). Methods Mutyh(-/-)and wild-type(WT)mice were used for the modeling of oxygen-induced retinopathy.The retinal oxidative stress was examined,and the ultrastructures of photoreceptors and mitochondria were observed.
View Article and Find Full Text PDFContributing factors to the oxidation-induced mutational landscape in human cells.
Nat Commun
December 2024
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT, 05405, USA.
8-oxoguanine (8-oxoG) is a common oxidative DNA lesion that causes G > T substitutions. Determinants of local and regional differences in 8-oxoG-induced mutability across genomes are currently unknown. Here, we show DNA oxidation induces G > T substitutions and insertion/deletion (INDEL) mutations in human cells and cancers.
View Article and Find Full Text PDFGenomic 8-oxoguanine modulates gene transcription independent of its repair by DNA glycosylases OGG1 and MUTYH.
Redox Biol
February 2025
Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, 7491, Trondheim, Norway; Department of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, 7006, Trondheim, Norway. Electronic address:
8-oxo-7,8-dihydroguanine (OG) is one of the most abundant oxidative lesions in the genome and is associated with genome instability. Its mutagenic potential is counteracted by a concerted action of 8-oxoguanine DNA glycosylase (OGG1) and mutY homolog DNA glycosylase (MUTYH). It has been suggested that OG and its repair has epigenetic-like properties and mediates transcription, but genome-wide evidence of this interdependence is lacking.
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