ReviewFuture oncology (London, England)2012
Medulloblastoma biology in the post-genomic era.
Review in Future oncology (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Clinicopathological insights of supratentorial embryonal tumor with medulloblastoma-like histopathology in adulthood: A case report.Biomedical reports · 2025Article
- An Update of Epigenetic Drugs for the Treatment of Cancers and Brain Diseases: A Comprehensive Review.Genes · 2023Review
- β-arrestin1-mediated acetylation of Gli1 regulates Hedgehog/Gli signaling and modulates self-renewal of SHH medulloblastoma cancer stem cells.BMC cancer · 2017Article
- Medulloblastoma: Molecular Classification-Based Personal Therapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Medulloblastomas, the most common malignant pediatric brain tumors, are comprised of four molecularly distinct subtypes. However, treatment has yet to exploit these molecular vulnerabilities. Three recent studies sequenced a total of 310 primary tumors and identified that two of the four medulloblastoma subtypes are concomitantly associated with subtype-specific mutations as previously characterized. In contrast, the overwhelming majority of mutations occurred only once in the entire cohort and just 12 genes were recurrently mutated with statistical significance. Perturbations in epigenetic regulation are emerging as a unifying theme in cancer and similarly recurring mutations in epigenetic mechanisms were distributed across all subtypes in medulloblastoma. Designing targeted therapies to such a molecularly diverse disease in the post-genomic era presents new challenges. This will require novel methods to link these nonrecurrent mutations into pathways, and preclinical models that faithfully recapitulate patient driver events. Presently, medulloblastoma reinforces epigenetic mechanisms as a tantalizing therapeutic target in cancers.
Indexed as
Identifiers
What OpenQuestion holds
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.