ArticleCurrent medicinal chemistry2026
Predicting Clinical Outcomes and Immunotherapy Responses in Lung Adenocarcinoma Based on Nicotine Response Characteristics.
Article in Current medicinal chemistry, 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
introductionNicotine facilitates the progression of Lung Adenocarcinoma (LUAD) by activating signaling pathways and remodeling the Tumor Microenvironment (TME). However, the molecular classification based on nicotine response spectrum and its clinical relevance remained unclear. MATERIALS AND
methodsWe retrieved 52 nicotine response-related genes from the MSigDB database and analyzed RNA-seq data obtained from TCGA-LUAD and GSE31210 cohorts. Distinct molecular subtypes were identified by consensus clustering analysis. Next, differential gene expression analysis and functional enrichment analysis were conducted. A prognostic RiskScore model was constructed using LASSO and Cox regression, and validated via Kaplan-Meier and ROC analyses. Immune microenvironment features were assessed using CIBERSORT, ESTIMATE, and TIDE algorithms, while pathway associations were explored via GSEA.
resultsTwo distinct molecular subtypes (C1 and C2) were identified, with C1 showing a more favorable prognosis. A RiskScore model developed based on five genes DISCUSSION: This study was the first to classify nicotine response-related molecular subtypes for LUAD, offering novel insights into nicotine-driven progression of LUAD. The RiskScore and nomogram may aid in risk stratification and personalized management, though further experimental validation is still needed.
conclusionThis study established a nicotine response-related prognostic model for LUAD, revealing its utility in predicting survival and immune therapy responses. Our findings provided novel biomarkers for personalized precision medicine in LUAD.
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