The effect of parotitis vaccine virus (strain L-3) on the DNA repair synthesis induced by 4-nitroquinoline-1-oxide has been studied. The efficiency of the repair synthesis depends on individual properties of the human body, viral multiplicity and concentration of the mutagen. A two-fold increase in DNA repair synthesis was obtained after infection of cells with low viral multiplicity (0.001 HADU50 per cell) and using 2.5 x 10(-7) M concentration of the mutagen A ten-fold increase in mutagen concentration affecting the infected cells was accompanied by the inhibition of DNA repair synthesis. Lymphocytes from children studied 7 days after vaccination by the attenuated virus did not reveal any changes in DNA repair synthesis as compared with the cells from nonvaccinated children.
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Mol Plant
January 2025
State Key Laboratory of Wheat Improvement, School of Advanced Agricultural Sciences, Peking University, Beijing 100871, China; Beijing Life Science Academy, Beijing 102299, China. Electronic address:
It has been hypothesized that DNA damage has the potential to induce DNA hypermethylation, contributing to carcinogenesis in mammals. However, there is no sufficient evidence to support that DNA damage can cause genome-wide DNA hypermethylation. Here, we demonstrated that DNA single-strand breaks with 3'-blocked ends (DNA 3'-blocks) can not only reinforce DNA methylation at normally methylated loci but also can induce DNA methylation at normally nonmethylated loci in plants.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Background: Ovarian cancer (OC), particularly high-grade serous ovarian carcinoma (HGSOC), is the leading cause of mortality from gynecological malignancies worldwide. Despite the initial effectiveness of treatment, acquired resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) represents a major challenge for the clinical management of HGSOC, highlighting the necessity for the development of novel therapeutic strategies. This study investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a pivotal regulator of glycolysis, in PARPi resistance and explored its potential as a therapeutic target to overcome PARPi resistance.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Gastrointestinal Surgery I Section, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Background: Gastric cancer peritoneal metastasis lacks effective predictive indices. This article retrospectively explored predictive values of DNA ploidy, stroma, and nucleotyping in gastric cancer peritoneal metastasis.
Methods: A comprehensive analysis was conducted on specimens obtained from 80 gastric cancer patients who underwent gastric resection at the Department of Gastrointestinal Surgery of Wuhan University Renmin Hospital.
Sci Rep
January 2025
Department of Electrical Electronical Engineering, Yaşar University, Bornova, İzmir, Turkey.
We aimed to build a robust classifier for the MGMT methylation status of glioblastoma in multiparametric MRI. We focused on multi-habitat deep image descriptors as our basic focus. A subset of the BRATS 2021 MGMT methylation dataset containing both MGMT class labels and segmentation masks was used.
View Article and Find Full Text PDFNat Commun
January 2025
Robson DNA Science Centre, Charbonneau Cancer Institute, Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
To tolerate oxidative stress, cells enable DNA repair responses often sensitive to poly(ADP-ribose) (PAR) polymerase 1 and 2 (PARP1/2) inhibition-an intervention effective against cancers lacking BRCA1/2. Here, we demonstrate that mutating the CHD6 chromatin remodeler sensitizes cells to PARP1/2 inhibitors in a manner distinct from BRCA1, and that CHD6 recruitment to DNA damage requires cooperation between PAR- and DNA-binding domains essential for nucleosome sliding activity. CHD6 displays direct PAR-binding, interacts with PARP-1 and other PAR-associated proteins, and combined DNA- and PAR-binding loss eliminates CHD6 relocalization to DNA damage.
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