ArticleTranslational cancer research2026
Chromatin remodeling-driven stratification and a five-gene RiskScore define proliferative aggressiveness and therapeutic vulnerabilities in neuroblastoma.
Article in Translational cancer research, 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
Background: Neuroblastoma is clinically heterogeneous, and epigenetic dysregulation-particularly chromatin remodeling-may organize aggressive tumor states and inform prognosis and therapeutic opportunities. This study aimed to define chromatin remodeling-associated neuroblastoma subtypes and develop a robust, biologically interpretable prognostic risk score derived from subtype-associated transcriptional changes, with external validation and functional characterization. Methods: A curated chromatin remodeling gene set was analyzed in RNA sequencing (RNA-seq) cohorts. Consensus clustering defined molecular subtypes in GSE62564 (n=498). Differential expression between subtypes [adjusted P value <0.05, |log fold change (FC)| ≥1] were screened by least absolute shrinkage and selection operator (LASSO) Cox regression. Collinearity control and multivariable Cox refinement yielded a five-gene signature. The RiskScore was evaluated by Kaplan-Meier analysis and time-dependent receiver operating characteristic (ROC) in GSE62564 and externally validated in GSE181559 (n=97) and FWR144 (n=144). Pathway analyses, transcription factor (TF) activity inference, and in silico drug sensitivity prediction were performed to support biological interpretation and therapeutic hypotheses. Results: Chromatin remodeling-based clustering stratified patients into prognostically distinct subtypes. The five-gene RiskScore robustly discriminated overall survival (OS) and achieved favorable time-dependent area under the curve (AUC) in the development cohort, remaining prognostic in both external cohorts. High-RiskScore tumors exhibited enhanced cell-cycle and DNA repair-related programs, consistent with a proliferative tumor-intrinsic aggressive phenotype. Drug sensitivity prediction suggested candidate vulnerabilities concordant with these mechanisms. Conclusions: Chromatin remodeling programs define reproducible neuroblastoma subtypes and support a stable five-gene prognostic RiskScore with external validation, linking aggressive biology to mechanistic pathways and therapeutic hypotheses.
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