ArticleNeuro-oncology2010
Genome-wide profiling using single-nucleotide polymorphism arrays identifies novel chromosomal imbalances in pediatric glioblastomas.
Article in Neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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
43 citing papers in PubMed, 104 citations in OpenAlex.
- Prognostic Relevance of Treatment Failure Patterns in Pediatric High-Grade Glioma: Is There a Role for a Revised Failure Classification System?International journal of radiation oncology, biology, physics · 2017Trial
- Applications of chemical exchange saturation transfer magnetic resonance imaging in identifying genetic markers in gliomas.NMR in biomedicine · 2023Review
- New natural compound inhibitors of PDGFRA (platelet-derived growth factor receptor α) based on computational study for high-grade glioma therapy.Frontiers in neuroscience · 2022Article
- Receptor tyrosine kinase (RTK) targeting in pediatric high-grade glioma and diffuse midline glioma: Pre-clinical models and precision medicine.Frontiers in oncology · 2022Review
- The Risk of Heart Disease-Related Death Among Anaplastic Astrocytoma Patients After Chemotherapy: A SEER Population-Based Analysis.Frontiers in oncology · 2022Article
- Prognosis of Oligodendroglioma Patients Stratified by Age: A SEER Population-Based Analysis.International journal of general medicine · 2021Article
- Establishment of age group classification for risk stratification in glioma patients.BMC neurology · 2020Article
- High-grade gliomas in adolescents and young adults highlight histomolecular differences from their adult and pediatric counterparts.Neuro-oncology · 2020Article
- H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3 and is essential for glioma tumorigenesis.Nature communications · 2019Article
- Mutation profiling of anaplastic ependymoma grade III by Ion Proton next generation DNA sequencing.F1000Research · 2019Article
- H3.3Cancer cell · 2017Article
- Molecular Basis of Pediatric Brain Tumors.Neuromolecular medicine · 2017Review
- Diffuse Intrinsic Pontine Glioma: New Pathophysiological Insights and Emerging Therapeutic Targets.Current neuropharmacology · 2017Review
- Review
- Characterization of copy number alterations in a mouse model of fibrosis-associated hepatocellular carcinoma reveals concordance with human disease.Cancer medicine · 2016Article
- Biopsy in a series of 130 pediatric diffuse intrinsic Pontine gliomas.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2015Article
- A preclinical study demonstrating the efficacy of nilotinib in inhibiting the growth of pediatric high-grade glioma.Journal of neuro-oncology · 2015Article
- Epigenetic dysregulation: a novel pathway of oncogenesis in pediatric brain tumors.Acta neuropathologica · 2014Review
- The genetic signatures of pediatric high-grade glioma: no longer a one-act play.Seminars in radiation oncology · 2014Review
- Unique genetic and epigenetic mechanisms driving paediatric diffuse high-grade glioma.Nature reviews. Cancer · 2014Review
Corrections and comments
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Authors and funding
19 authors at 8 institutions in 3 countries.
Funding
Abstract
Available data on genetic events in pediatric grade IV astrocytomas (glioblastoma [pGBM]) are scarce. This has traditionally been a major impediment in understanding the pathogenesis of this tumor and in developing ways for more effective management. Our aim is to chart DNA copy number aberrations (CNAs) and get insight into genetic pathways involved in pGBM. Using the Illumina Infinium Human-1 bead-chip-array (100K single-nucleotide polymorphisms [SNPs]), we genotyped 18 pediatric and 6 adult GBMs. Results were compared to BAC-array profiles harvested on 16 of the same pGBM, to an independent data set of 9 pediatric high-grade astrocytomas (HGAs) analyzed on Affymetrix 250K-SNP arrays, and to existing data sets on HGAs. CNAs were additionally validated by real-time qPCR in a set of genes in pGBM. Our results identify with nonrandom clustering of CNAs in several novel, previously not reported, genomic regions, suggesting that alterations in tumor suppressors and genes involved in the regulation of RNA processing and the cell cycle are major events in the pathogenesis of pGBM. Most regions were distinct from CNAs in aGBMs and show an unexpectedly low frequency of genetic amplification and homozygous deletions and a high frequency of loss of heterozygosity for a high-grade I rapidly dividing tumor. This first, complete, high-resolution profiling of the tumor cell genome fills an important gap in studies on pGBM. It ultimately guides the mapping of oncogenic networks unique to pGBM, identification of the related therapeutic predictors and targets, and development of more effective therapies. It further shows that, despite commonalities in a few CNAs, pGBM and aGBMs are two different diseases.
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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.