ArticleNeuro-oncology2022
Intratumoral heterogeneity of MYC drives medulloblastoma metastasis and angiogenesis.
Article in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- p53 wild-type/low c-Myc-expressing ONS76 pediatric medulloblastoma cells become senescent after gamma-irradiation and can be eliminated by senolytic substances.Cell death discovery · 2026Article
- From developmental origins to relapse: molecular and therapeutic insights in medulloblastoma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026Review
- Metabolic Landscape and Emerging Therapeutic Potential in Pediatric and Adult Gliomas.International journal of molecular sciences · 2026Review
- Exploring the lactate-metabolism related characteristics during the development of medulloblastoma through single-cell and bulk RNA-seq.Translational cancer research · 2026Article
- Strength through diversity: how cancers thrive when clones cooperate.Molecular oncology · 2026Review
- Reprogramming the tumor microenvironment with c-MYC-based gene circuit platform to enhance specific cancer immunotherapy.Nature communications · 2025Article
- The EIF4EBP1 gene encoding 4EBP1 is transcriptionally upregulated by MYC and linked to shorter survival in medulloblastoma.Cell death discovery · 2025Article
- Beyond the Limit: MYC Mediates Tumor Immune Escape.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Alpha/beta values in pediatric medulloblastoma: implications for tailored approaches in radiation oncology.Radiation oncology (London, England) · 2025Article
- MYC overexpression and SMARCA4 loss cooperate to drive medulloblastoma formation in mice.Acta neuropathologica communications · 2023Article
- Review
- Cancer Stem Cells in Tumours of the Central Nervous System in Children: A Comprehensive Review.Cancers · 2023Review
- ZEB1 is a Subgroup-Specific Marker of Prognosis and Potential Drug Target in Medulloblastoma.Neuromolecular medicine · 2023Article
- AMPK attenuates SHH subgroup medulloblastoma growth and metastasis by inhibiting NF-κB activation.Cell & bioscience · 2023Article
- Nucleolin recognizing silica nanoparticles inhibit cell proliferation by activating the Bax/Bcl-2/caspase-3 signalling pathway to induce apoptosis in liver cancer.Frontiers in pharmacology · 2023Article
- Review
- High expression of hypoxia-inducible factor 1-alpha predicts poor prognosis in pancreatic ductal adenocarcinoma: a meta-analysis and database validation protocol.Translational cancer research · 2022Article
- Pathological implications of metabolic reprogramming and its therapeutic potential in medulloblastoma.Frontiers in cell and developmental biology · 2022Review
- UBE2C promotes leptomeningeal dissemination and is a therapeutic target in brain metastatic disease.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
28 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntratumoral heterogeneity is crucially involved in metastasis, resistance to therapy, and cancer relapse. Amplifications of the proto-oncogene MYC display notable heterogeneity at the single-cell level and are associated with a particularly dismal prognosis in high-risk medulloblastomas (MBs). The aim of this study was to establish the relevance of interclonal cross-talk between MYC-driven and non-MYC-driven MB cells.
methodsWe used fluorescence in situ hybridization, single-cell transcriptomics, and immunohistochemistry, in vitro isogenic cell models, non-targeted proteomics, mass spectrometry-based metabolite quantification, HUVECs tube formation assay, and orthotopic in vivo experiments to investigate interclonal cross-talk in MB.
resultsWe found that the release of lactate dehydrogenase A (LDHA) from MYC-driven cells facilitates metastatic seeding and outgrowth, while secretion of dickkopf WNT signaling pathway inhibitor 3 from non-MYC-driven cells promotes tumor angiogenesis. This tumor-supporting interaction between both subclones was abrogated by targeting the secretome through pharmacological and genetic inhibition of LDHA, which significantly suppressed tumor cell migration.
conclusionOur study reveals the functional relevance of clonal diversity and highlights the therapeutic potential of targeting the secretome to interrupt interclonal communication and progression in high-risk MB.
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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 Socratic graph.