ArticleMolecular oncology2023
Multi-omic integration of DNA methylation and gene expression data reveals molecular vulnerabilities in glioblastoma.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- A Vascular-Extracellular Matrix Molecular Program Identifies High-Risk Diffuse Glioma Across Independent Multi-Omics.Cancers · 2026Article
- Modeling glioblastoma relapse in vitro: a critical journey from 2D models to organ-on-chip alternatives.NPJ precision oncology · 2026Review
- A cellular epigenetic classification system for glioblastoma.Neuro-oncology · 2026Article
- Multi-Omics Integration for Advancing Glioma Precision Medicine.Annals of clinical and translational neurology · 2026Review
- Transcriptional dynamics of CD8Molecular cancer · 2025Article
- Toward Artificial Intelligence in Oncology and Cardiology: A Narrative Review of Systems, Challenges, and Opportunities.Journal of clinical medicine · 2025Article
- Coordinated Transcriptomic and Epigenetic Approach Reveals Molecular Features Underlying Natural Mating Ability in Captive Male Giant Pandas.Ecology and evolution · 2025Article
- MOTL: enhancing multi-omics matrix factorization with transfer learning.Genome biology · 2025Article
- DNMT3B aggravated renal fibrosis in diabetic kidney disease via activating Wnt/β-catenin signaling pathway.Scientific reports · 2025Article
- Peripheral blood-derived immune cell counts as prognostic indicators and their relationship with DNA methylation subclasses in glioblastoma patients.Brain pathology (Zurich, Switzerland) · 2025Article
- A coregulatory influence map of glioblastoma heterogeneity and plasticity.NPJ precision oncology · 2025Article
- Integration of multi-omics layers empowers precision diagnosis through unveiling pathogenic mechanisms on maple syrup urine disease.Journal of inherited metabolic disease · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is one of the most aggressive types of cancer and exhibits profound genetic and epigenetic heterogeneity, making the development of an effective treatment a major challenge. The recent incorporation of molecular features into the diagnosis of patients with GBM has led to an improved categorization into various tumour subtypes with different prognoses and disease management. In this work, we have exploited the benefits of genome-wide multi-omic approaches to identify potential molecular vulnerabilities existing in patients with GBM. Integration of gene expression and DNA methylation data from both bulk GBM and patient-derived GBM stem cell lines has revealed the presence of major sources of GBM variability, pinpointing subtype-specific tumour vulnerabilities amenable to pharmacological interventions. In this sense, inhibition of the AP-1, SMAD3 and RUNX1/RUNX2 pathways, in combination or not with the chemotherapeutic agent temozolomide, led to the subtype-specific impairment of tumour growth, particularly in the context of the aggressive, mesenchymal-like subtype. These results emphasize the involvement of these molecular pathways in the development of GBM and have potential implications for the development of personalized therapeutic approaches.
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