ArticleFrontiers in oncology2026
Discovery and validation of a robust 11-gene prognostic signature via integrative multi-omics profiling in VD-CAG-treated non-M3 AML.
Article in Frontiers in oncology, 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
Objectives: While the venetoclax-based VD-CAG regimen has shown promising efficacy in acute myeloid leukemia (AML), its underlying molecular response mechanisms remain poorly understood, and robust prognostic biomarkers for non-M3 AML treated with this regimen are lacking. This study aimed to elucidate the molecular alterations associated with VD-CAG treatment response, and to identify and validate robust prognostic biomarkers to improve risk stratification for non-M3 AML patients. Methods: This study enrolled 15 non-M3 AML patients receiving VD-CAG induction therapy, and conducted integrative multi-omics profiling of their bone marrow samples: RNA sequencing was performed on 10 pairs of pre- and post-treatment samples, while data-independent acquisition (DIA) proteomics was applied to another 5 paired samples. Weighted gene co-expression network analysis (WGCNA) was used to identify gene modules correlated with composite complete remission. A prognostic signature was further derived using Least Absolute Shrinkage and Selection Operator (LASSO) regression, with the TCGA-LAML cohort as the discovery set and the independent Beat AML cohort as the external validation set. Results: Transcriptomic analysis revealed that differentially expressed genes after VD-CAG treatment were mainly enriched in MAPK signaling and cell adhesion pathways. WGCNA identified five gene modules significantly correlated with treatment remission. We finally constructed a robust 11-gene prognostic signature ( Conclusions: This study reveals the molecular alterations associated with VD-CAG treatment in non-M3 AML, and provides a validated 11-gene prognostic signature. These findings enhance our understanding of the response mechanisms of the VD-CAG regimen, and offer a tool to improve prognostic stratification and clinical decision-making for non-M3 AML patients.
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