ArticleGenes & development2010
Pleiotropic role for MYCN in medulloblastoma.
Article in Genes & development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
120 citing papers in PubMed, 174 citations in OpenAlex.
- [EJNMMI research · 2026Article
- A tumor-associated photoreceptor signature unifies distinct central nervous system malignancies.Cancer cell · 2026Article
- Medulloblastoma in Adolescents and Young Adults: Molecular Subgroups, Prognostic Biomarkers, and Age-Specific Therapeutic Challenges.Current issues in molecular biology · 2026Review
- PLK1 inhibition by volasertib suppresses key transcriptional regulators underlying fibroblast activation and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Investigation of a global mouse methylome atlas reveals subtype-specific copy number alterations in pediatric cancer models.Nature genetics · 2026Article
- The transcription factor LHX2 mediates and enhances oncogenic BMP signaling in medulloblastoma.Cell death and differentiation · 2025Article
- Identification of a small molecule targeting EPLIN as a novel strategy for the treatment of pediatric neuroblastoma and medulloblastoma.Cell death & disease · 2025Article
- Heterozygous Kmt2d loss diminishes enhancers to render medulloblastoma cells vulnerable to combinatory inhibition of LSD1 and OXPHOS.Cell reports · 2025Article
- MYC-dependent upregulation of the de novo serine and glycine synthesis pathway is a targetable metabolic vulnerability in group 3 medulloblastoma.Neuro-oncology · 2025Article
- Arrested development: the dysfunctional life history of medulloblastoma.Genes & development · 2025Review
- DHODH Inhibition SuppressesCancers · 2024Article
- Drivers Underlying Metastasis and Relapse in Medulloblastoma and Targeting Strategies.Cancers · 2024Review
- Group 3 medulloblastoma transcriptional networks collapse under domain specific EP300/CBP inhibition.Nature communications · 2024Article
- Preclinical pediatric brain tumor models for immunotherapy: Hurdles and a way forward.Neuro-oncology · 2024Review
- MYCN in human development and diseases.Frontiers in oncology · 2024Review
- Mouse models of pediatric high-grade gliomas with MYCN amplification reveal intratumoral heterogeneity and lineage signatures.Nature communications · 2023Article
- A MYCN-independent mechanism mediating secretome reprogramming and metastasis inScience advances · 2023Article
- ARF suppression by MYC but not MYCN confers increased malignancy of aggressive pediatric brain tumors.Nature communications · 2023Article
- Targeting protein folding in N-Myc-driven medulloblastoma.Molecular oncology · 2023Article
- N-myc-Mediated Translation Control Is a Therapeutic Vulnerability in Medulloblastoma.Cancer research · 2023Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 6 institutions in 4 countries.
Funding
Abstract
Medulloblastoma (MB) is the most common malignant brain tumor of childhood. Sonic Hedgehog (SHH) signaling drives a minority of MB, correlating with desmoplastic pathology and favorable outcome. The majority, however, arises independently of SHH and displays classic or large cell anaplastic (LCA) pathology and poor prognosis. To identify common signaling abnormalities, we profiled mRNA, demonstrating misexpression of MYCN in the majority of human MB and negligible expression in normal cerebella. We clarified a role in pathogenesis by targeting MYCN (and luciferase) to cerebella of transgenic mice. MYCN-driven MB showed either classic or LCA pathologies, with Shh signaling activated in approximately 5% of tumors, demonstrating that MYCN can drive MB independently of Shh. MB arose at high penetrance, consistent with a role for MYCN in initiation. Tumor burden correlated with bioluminescence, with rare metastatic spread to the leptomeninges, suggesting roles for MYCN in both progression and metastasis. Transient pharmacological down-regulation of MYCN led to both clearance and senescence of tumor cells, and improved survival. Targeted expression of MYCN thus contributes to initiation, progression, and maintenance of MB, suggesting a central role for MYCN in pathogenesis.
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Registered trials
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.