Role of MYC in medulloblastoma
Open accessAbstract
Since its discovery as an oncogene carried by the avian acute leukemia virus MC29 in myelocytomatosis (Roussel et al. 1979) and its cloning (Vennstrom et al. 1982), c-MYC (MYC), as well as its paralogs MYCN and MYCL1, has been shown to play essential roles in cycling progenitor cells born from proliferating zones during embryonic development, and in all proliferating cells after birth. MYC deletion induces cell-cycle exit or cell death, depending on the cell type and milieu, whereas MYC and MYCN amplification or overexpression promotes cell proliferation and occurs in many cancers. Here, we review the relationship of MYC family proteins to the four molecularly distinct medulloblastoma subgroups, discuss the possible roles MYC plays in each of these subgroups and in the developing cells of the posterior fossa, and speculate on possible therapeutic strategies targeting MYC.
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MYC amplifications, G3 molecular group, and presence of metastatic disease-but not iso17-are key prognostic indicators of poor outcome in G3 and G4 cases across a population treated with standard regimens.
“This analysis confirms MYC amplifications, G3 molecular group, and the presence of metastatic disease—but not iso17—as key prognostic indicators of poor outcome in G3 and G4 cases across a population of patients with medulloblastoma treated with standard regimens (20, 21).”
From The Medulloblastoma Meta-Analysis Portal Enables Integrative Exploration of Clinical and Genomic Data from Patients (2025) · cites this paper as [21]
The sections “MYC and the Medulloblastoma Subgroups” and “MYC in the Group 3 Subgroup” link MYC amplification and Group 3 disease to aggressive tumors and poor survival, and report that metastases are especially prevalent in Group 3. They do not establish metastatic disease as a prognostic indicator in Group 3 and 4 patients treated with standard regimens, or assess the claim that iso17 is not one. Page numbers are not available in our copy. (LLM, conf=0.86)
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References 103 · Cited by 180
Research works printed but not linked: 2
- [8]8. Ã Campbell KJ, White RJ. 2013. MYC regulation of cell growth through control of RNA polymerae I and III activities. Cold Spring Harb Perspect Med doi: 10.1101/cshper- spect.a018408. · DOI
- [68]68. Ã Rahl PB, Young RA. 2013. Myc and transcription elonga- tion. Cold Spring Harb Perspect Med doi: 10.1101/cshper- spect.a014340. · DOI
- Authors
- Roussel, M. F., & Robinson, G. W.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-11-01
- Volume
- 3
- Issue
- 11
- Pages
- a014308-a014308
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC3808772
- OpenAlex
- W2168957937
- Cited by
- 180
- References
- 103
- Citations by year
- 2026: 6 · 2025: 20 · 2024: 13 · 2023: 17 · 2022: 10 · 2021: 25 · 2020: 16 · 2019: 10 · 2018: 15 · 2017: 8 · 2016: 13 · 2015: 10 · 2014: 14 · 2013: 3
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- St. Jude Children's Research Hospital (CA21765)
- National Institutes of Health (CA21765), CA096832)
- National Cancer Institute (CA 096832, CA21765, P01CA096832, P30CA021765)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Neurology › Neuroblastoma Research and Treatments
- Keywords
- c-Myc, medulloblastoma, MYCN, MYCL1, cell proliferation, cell cycle exit, MYC-targeted therapy, oncogenes
- MeSH terms
- Cerebellar Neoplasms, Cranial Fossa, Posterior, Gene Amplification, Humans, Medulloblastoma, Genes, myc, Proto-Oncogene Proteins c-myc, MicroRNAs, Epigenesis, Genetic
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