ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Investigating the role of inflammatory bowel disease-associated gene expression in oral cancer using single-cell RNA sequencing.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeThis study aimed to investigate the expression of infl ammatory bowel disease (IBD)-associated genes in oral cancer and to elucidate the cellular and molecular pathways that may serve as potential therapeutic targets. METHODS/PATIENTS: Oral cancer tissue samples were subjected to single-cell RNA sequencing to characterize cell clusters and gene expression patterns. UMAP and t-SNE were used for dimensionality reduction and visualization of cellular subgroups. Dot plots were applied to identify key gene expression signatures. Gene Set Enrichment Analysis (GSEA) was performed to examine pathways associated with NFKBIA expression.
resultsSingle-cell analysis revealed heterogeneous cell populations, including T cells, fi broblasts, and malignant cells. Diff erential expression analysis identifi ed elevated levels of LYZ and IL7R in specifi c cell subsets. In several clusters, IBD-related genes such as NFKBIA, RB1CC1, and ATG5 were upregulated. GSEA indicated that NFKBIA expression was signifi cantly associated with the chemokine-mediatedsignaling pathway, a process implicated in tumor growth.
conclusionsThis study highlights the cellular heterogeneity and distinct gene expression programs inoral cancer, emphasizing the relevance of IBD-associated genes. The association between NFKBIA expression and chemokine-mediated signaling provides insights that may contribute to the development of personalized therapeutic strategies for IBD-related mechanisms in oral cancer.
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