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The overall survival of patients with lower grade glioma (LGG) that might develop into high-grade malignant glioma shows marked heterogeneity. The currently used clinical evaluation index is not sufficient to predict precise prognostic outcomes accurately. To optimize survival risk stratification and the personalized management of patients with LGG, there is an urgent need to develop an accurate risk prediction model. The TCGA-LGG dataset, downloaded from The Cancer Genome Atlas (TCGA) portal, was used as a training cohort, and the Chinese Glioma Genome Atlas (CGGA) dataset and Rembrandt dataset were used as validation cohorts. The levels of various cancer hallmarks were quantified, which identified glycolysis as the primary overall survival-related risk factor in LGGs. Furthermore, using various bioinformatic and statistical methods, we developed a strong glycolysis-related gene signature to predict prognosis. Gene set enrichment analysis showed that in our model, high-risk glioma correlated with the chemoradiotherapy resistance and poor survival. Moreover, based on established risk model and other clinical features, a decision tree and a nomogram were built, which could serve as useful tools in the diagnosis and treatment of LGGs. This study indicates that the glycolysis-related gene signature could distinguish high-risk and low-risk patients precisely, and thus can be used as an independent clinical feature.
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http://dx.doi.org/10.3389/fgene.2022.843711 | DOI Listing |
ACS Biomater Sci Eng
September 2025
Materials Engineering, McGill university, Montreal H3A0C5, Canada.
Transcutaneous devices such as dental implants frequently fail due to infections at their interfaces with epithelial tissues. These infections are facilitated by the lack of integration between the devices and the surrounding soft tissues. This study aims to improve epithelial integration through surface modification of a transcutaneous implant material (polyetheretherketone (PEEK)).
View Article and Find Full Text PDFNucleic Acids Res
September 2025
Université Paris-Saclay, INRAE, AgroParisTech, Institut Jean-Pierre Bourgin for Plant Sciences (IJPB), 78000 Versailles, France.
BRCA2 is crucial for mediating homology-directed DNA repair (HDR) through its binding to single-stranded DNA (ssDNA) and the recombinases RAD51 and DMC1. Most BRCA2 orthologs have a canonical DNA-binding domain (DBD) with the exception of Drosophila melanogaster. It remains unclear whether such a noncanonical BRCA2 variant without DBD possesses a DNA-binding activity.
View Article and Find Full Text PDFJ Pathol
September 2025
Department of Biomedical Sciences, Cornell University, Ithaca, NY, USA.
Serous endometrial carcinoma (SEC) is one of the most lethal types of uterine cancer, responsible for about 40% of all endometrial cancer-related deaths. Cell state dynamics during the early stages of SEC remain largely unknown, thereby hindering early detection and treatment of this disease. Here, we provide a comprehensive census of cell types and their states for normal, predysplastic, and dysplastic endometrium in a genetic mouse model of SEC.
View Article and Find Full Text PDFCancer Biol Med
September 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Objective: The key molecular events signifying the -induced gastric carcinogenesis process are largely unknown.
Methods: Bulk tissue-proteomics profiling were leveraged across multi-stage gastric lesions from Linqu ( = 166) and Beijing sets ( = 99) and single-cell transcriptomic profiling ( = 18) to decipher key molecular signatures of -related gastric lesion progression and gastric cancer (GC) development. The association of key proteins association with gastric lesion progression and GC development were prospectively studied building on follow-up of the Linqu set and UK Biobank ( = 48,529).
Background: Intervertebral disc degeneration (IDD) is a prevalent spinal condition frequently associated with pain and motor impairment, imposing a substantial burden on quality of life. Despite extensive investigations into the genetic predisposition to IDD, the precise pathogenic genes and molecular pathways involved remain inadequately characterized, underscoring the need for continued research to clarify its genetic underpinnings.
Methods: This study leveraged IDD data from the FinnGen R12 cohort and integrated expression quantitative trait loci data across 49 tissues from the Genotype-Tissue Expression version 8 database to perform a cross-tissue transcriptome-wide association study (TWAS).