ArticleCancer cell2024
Integrated proteogenomic characterization of glioblastoma evolution.
Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 79 citations in OpenAlex.
- Functional proteomic and phosphoproteomic profiling of routine FFPE CNS tumor tissue complements genomic and epigenomic characterization.Acta neuropathologica · 2026Article
- LRIG2 suppresses NK cell-induced GSDME-mediated pyroptosis via the LAMP1-STAT3 pathway in glioma.Journal for immunotherapy of cancer · 2026Article
- Glioblastoma recurrence: An NGS-centered seed-soil framework.Neoplasia (New York, N.Y.) · 2026Article
- Systems biology of Wnt signaling in glioma chemotherapy resistance: Integrating multi-omics mechanisms and emerging therapeutic vulnerabilities (Review).Oncology letters · 2026Review
- Enabling Variant Proteogenomic Assay Development Through a Peptide Target Selection Pipeline and Web Application.Proteomics · 2026Article
- The Invasive Margin of Glioblastoma as a Molecular Ecosystem: Spatial Heterogeneity, Tumor-Host Interactions, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Development of K-CORE: a web-based platform for integrated clinico-genomic analysis.Life science alliance · 2026Article
- Patient-derived organoids predict personalized drug response and reveal alternative therapeutic options in glioblastoma.Cell reports. Medicine · 2026Article
- Spatial Omics Technologies in Glioblastoma Research: Principles, Applications, and Best Practices.Genes · 2026Review
- LFPM inhibition of RING1-mediated p53Cell death and differentiation · 2026Article
- Single-cell transcriptomics reveals MAFB-driven macrophage reprogramming and immune divergence in recurrent glioblastoma.BMC cancer · 2026Article
- Decoding glioblastoma evolution and heterogeneity through mechanistic modeling: implications for clinical translation.Journal of experimental & clinical cancer research : CR · 2026Review
- Role of NR2F2-mediated reprogramming of endothelial cells in glioblastoma progression.iScience · 2026Article
- Inferring translational efficiency from transcriptomes improves noncanonical neoantigen prioritization and cancer patient stratification.NPJ precision oncology · 2026Article
- T2Pdecoder enables protein-centric analyses from transcriptomic data.Nature communications · 2026Article
- Ligand-dependent corepressor suppresses angiogenesis and macrophage infiltration in gliobl astoma microenvironment via MCP-1 down-regulation.BMC biotechnology · 2026Article
- Copper transporters promote the malignant progression of glioblastoma by regulating the immunosuppressive tumour microenvironment via the SLC31A1-WNT5A axis.Journal of translational medicine · 2026Article
- Discovering proteo-transcriptomic networks via biologically informed heterogeneous graph learning.Nucleic acids research · 2026Article
- Proteogenomic decoding of chemotherapy resistance in patients with triple-negative breast cancer.Genome biology · 2026Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
39 authors at 13 institutions in 7 countries.
Funding
Abstract
The evolutionary trajectory of glioblastoma (GBM) is a multifaceted biological process that extends beyond genetic alterations alone. Here, we perform an integrative proteogenomic analysis of 123 longitudinal glioblastoma pairs and identify a highly proliferative cellular state at diagnosis and replacement by activation of neuronal transition and synaptogenic pathways in recurrent tumors. Proteomic and phosphoproteomic analyses reveal that the molecular transition to neuronal state at recurrence is marked by post-translational activation of the wingless-related integration site (WNT)/ planar cell polarity (PCP) signaling pathway and BRAF protein kinase. Consistently, multi-omic analysis of patient-derived xenograft (PDX) models mirror similar patterns of evolutionary trajectory. Inhibition of B-raf proto-oncogene (BRAF) kinase impairs both neuronal transition and migration capability of recurrent tumor cells, phenotypic hallmarks of post-therapy progression. Combinatorial treatment of temozolomide (TMZ) with BRAF inhibitor, vemurafenib, significantly extends the survival of PDX models. This study provides comprehensive insights into the biological mechanisms of glioblastoma evolution and treatment resistance, highlighting promising therapeutic strategies for clinical intervention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.