ReviewBrain pathology (Zurich, Switzerland)2013
The role of chromatin remodeling in medulloblastoma.
Review in Brain pathology (Zurich, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency.Nature genetics · 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
- Advancing Medulloblastoma Therapy in Pediatrics: Integrative Molecular Classification and Emerging Treatments.Brain sciences · 2025Review
- Review
- Arrested development: the dysfunctional life history of medulloblastoma.Genes & development · 2025Review
- The modification role and tumor association with a methyltransferase: KMT2C.Frontiers in immunology · 2024Review
- Article
- Epigenetics and immune cells in medulloblastoma.Frontiers in genetics · 2023Review
- A novel dual epigenetic approach targeting BET proteins and HDACs in Group 3 (MYC-driven) Medulloblastoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Evaluation of an EZH2 inhibitor in patient-derived orthotopic xenograft models of pediatric brain tumors alone and in combination with chemo- and radiation therapies.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- MiR-212-3p functions as a tumor suppressor gene in group 3 medulloblastoma via targeting nuclear factor I/B (NFIB).Acta neuropathologica communications · 2021Article
- Histone demethylase UTX/KDM6A enhances tumor immune cell recruitment, promotes differentiation and suppresses medulloblastoma.Cancer letters · 2021Article
- Downregulation of miR-326 and its host gene β-arrestin1 induces pro-survival activity of E2F1 and promotes medulloblastoma growth.Molecular oncology · 2021Article
- Medulloblastoma: "Onset of the molecular era".Molecular biology reports · 2020Review
- Clinical and mutational profiles of adult medulloblastoma groups.Acta neuropathologica communications · 2020Article
- Reliable tumor detection by whole-genome methylation sequencing of cell-free DNA in cerebrospinal fluid of pediatric medulloblastoma.Science advances · 2020Article
- Molecular Heterogeneity and Cellular Diversity: Implications for Precision Treatment in Medulloblastoma.Cancers · 2020Review
- Developmental origins and oncogenic pathways in malignant brain tumors.Wiley interdisciplinary reviews. Developmental biology · 2019Review
- Evaluation of Protein Kinase Inhibitors with PLK4 Cross-Over Potential in a Pre-Clinical Model of Cancer.International journal of molecular sciences · 2019Article
- Transcriptional repressor REST drives lineage stage-specific chromatin compaction atScience signaling · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The unexpectedly high frequency and universality of alterations to the chromatin machinery is one of the most striking themes emerging from the current deluge of cancer genomics data. Medulloblastoma (MB), a malignant pediatric brain tumor, is no exception to this trend, with a wealth of recent studies indicating multiple alterations at all levels of chromatin processing. MB is typically now regarded as being composed of four major molecular entities (WNT, SHH, Group 3 and Group 4), which vary in their clinical and biological characteristics. Similarities and differences across these subgroups are also reflected in the specific chromatin modifiers that are found to be altered in each group, and each new cancer genome sequence or microarray profile is adding to this important knowledge base. These data are fundamentally changing our understanding of tumor developmental pathways, not just for MB but also for cancer as a whole. They also provide a new class of targets for the development of rational, personalized therapeutic approaches. The mechanisms by which these chromatin remodelers are dysregulated in MB, and the consequences both for future basic research and for translation to the clinic, will be examined here.
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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.