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Genomic instability is a prominent hallmark of cancer, and Long non-coding RNAs (LncRNAs) have been implicated in cancer biology. This study aimed to develop a prognostic model for glioma by focusing on genomic instability-associated lncRNAs (GILnc). A computational framework was implemented to identify GILnc, followed by immuno-scoring and immune cell infiltration analyses using the ESTIMATE and CIBERSORT algorithms. Putative drugs and downstream target proteins were predicted using the Connectivity Map (Cmap) and STITCH database. Cox regression analysis was employed for prognostic modeling, and a competitive endogenous RNA (ceRNA) network was constructed using the miRcode database, miRDB, miRTarBase, and TargetScan. A set of GILnc was successfully identified in glioma, showing a significant correlation with prognosis. Based on GILnc, a 16-gene prognostic model (GILncSig) was developed to assess risk scores for glioma patients. A clinical-accessible and high-performance nomogram was formulated by integrating independent clinical parameters. Furthermore, several putative drugs with potential anti-tumor effects in genomically unstable glioma were identified. This study contributes novel insights into GILnc in gliomas and presents the GILncSig prognostic model with robust independent predictive capabilities. These findings offer valuable implications for personalized treatment strategies in glioma. The putative drug predictions provide promising avenues for therapeutic intervention in glioma patients with genomic instability. Overall, our research advances the understanding of lncRNA involvement in cancer genomic instability and establishes a basis for future investigations in this field.
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http://dx.doi.org/10.1002/ajmg.b.33044 | DOI Listing |
Hum Pathol
September 2025
Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. Electronic address:
Renal cell carcinoma (RCC) is a heterogeneous kidney malignancy driven by complex genetic, molecular, and metabolic alterations. Emerging evidence implicates centrosome dysfunction and autophagy dysregulation in RCC initiation, progression, and resistance to therapy. The centrosome plays a critical role in mitotic fidelity, and its dysfunction often leads to chromosomal and genomic instability.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Biosciences, JIS University, 81, Nilgunj Road, Agarpara, Kolkata, West Bengal 700109, India. Electronic address:
The malignant manifestation of breast cancer is driven by complex molecular alterations that extend beyond genetic mutations to include epigenetic dysregulation. Among these, DNA methylation is a critical and reversible epigenetic modification that significantly influences breast cancer initiation, progression, and therapeutic resistance. This process, mediated by DNA methyltransferases (DNMTs), involves the addition of methyl groups to cytosine residues within CpG dinucleotides, resulting in transcriptional repression of genes.
View Article and Find Full Text PDFNeurol Res
September 2025
Henan Provincial People's Hospital, Department of Surgery of Spine and Spinal Cord, People's Hospital of Zhengzhou University, Zhengzhou, China.
Background: Immunotherapy holds significant yet underexplored potential for low-grade glioma (LGG) treatment. We therefore interrogated the role of Fanconi Anemia Complementation Group C (FANCC) as a novel immune checkpoint regulator given its spatial correlation with tumor microenvironments and clinical associations with immunosuppressive markers.
Objectives: FANCC is implicated in various tumor progressions; its role in LGG remains unexplored.
Cancer Pathog Ther
September 2025
Department of Microbiology, SRM Medical College Hospital and Research Centre, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu, 603203, Tamil Nadu, India.
Oral cancer pathogenesis is significantly influenced by species, especially , through chronic inflammation and cellular dysregulation. Epidemiological studies highlight a strong correlation between persistent infections and oral carcinogenesis. Experimental evidence has identified key biomolecular mechanisms, including biofilm formation, epithelial invasion, and immune evasion.
View Article and Find Full Text PDFAPMIS
September 2025
Cancer Cytogenomic Laboratory, Center for Research and Drug Development (NPDM), Federal University of Ceara, Fortaleza, Ceara, Brazil.
Toll-like receptors (TLRs) are essential components of the innate immune system, functioning as pattern recognition receptors (PRRs) to detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). In hematological malignancies, particularly myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and chronic myeloid leukemia (CML), TLRs influence inflammation, disease progression, and therapeutic response. This review highlights the prognostic relevance of TLR expression, the role of the MyD88 signaling pathway in clonal evolution, and the dual nature of TLR-mediated immune responses, either promoting antitumor activity or contributing to leukemogenesis.
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