ArticleNeuro-oncology2005
Microarray analysis of pediatric ependymoma identifies a cluster of 112 candidate genes including four transcripts at 22q12.1-q13.3.
Article in Neuro-oncology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 70 citations in OpenAlex.
- Engine breakdown of lysosomes and related organelles and the resulting physiology.Frontiers in cell and developmental biology · 2025Review
- Optimizing outcomes in intracranial ependymoma: a contemporary review.Frontiers in oncology · 2025Review
- Review
- Integrative clinical and molecular characterization of translocation renal cell carcinoma.Cell reports · 2022Article
- A transient receptor potential channel-related model based on machine learning for evaluating tumor microenvironment and immunotherapeutic strategies in acute myeloid leukemia.Frontiers in immunology · 2022Article
- Review
- Context-dependent actions of Polycomb repressors in cancer.Oncogene · 2016Review
- IsoSeq analysis and functional annotation of the infratentorial ependymoma tumor tissue on PacBio RSII platform.Meta gene · 2016Article
- EphB2 activation is required for ependymoma development as well as inhibits differentiation and promotes proliferation of the transformed cell.Scientific reports · 2015Article
- Genomic characterization of ependymomas reveals 6q loss as the most common aberration.Oncology reports · 2014Article
- Tumor prognostic factors and the challenge of developing predictive factors.Current oncology reports · 2013Article
- Current treatment options for pediatric and adult patients with ependymoma.Current treatment options in oncology · 2012Article
- Chromosomal anomalies and prognostic markers for intracranial and spinal ependymomas.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2012Review
- A prognostic gene expression signature in infratentorial ependymoma.Acta neuropathologica · 2012Article
- The microtubule-associated protein EB1 maintains cell polarity through activation of protein kinase C.Biochemical and biophysical research communications · 2012Article
- Molecular genetics of ependymoma.Chinese journal of cancer · 2011Review
- Tumor profiling: development of prognostic and predictive factors to guide brain tumor treatment.Current oncology reports · 2011Review
- Article
- A clinically relevant orthotopic xenograft model of ependymoma that maintains the genomic signature of the primary tumor and preserves cancer stem cells in vivo.Neuro-oncology · 2010Article
- Ependymomas in adults.Current neurology and neuroscience reports · 2010Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ependymomas are glial cell-derived tumors characterized by varying degrees of chromosomal abnormalities and variability in clinical behavior. Cytogenetic analysis of pediatric ependymoma has failed to identify consistent patterns of abnormalities, with the exception of monosomy of 22 or structural abnormalities of 22q. In this study, a total of 19 pediatric ependymoma samples were used in a series of expression profiling, quantitative real-time PCR (Q-PCR), and loss of heterozygosity experiments to identify candidate genes involved in the development of this type of pediatric malignancy. Of the 12,627 genes analyzed, a subset of 112 genes emerged as being abnormally expressed when compared to three normal brain controls. Genes with increased expression included the oncogene WNT5A; the p53 homologue p63; and several cell cycle, cell adhesion, and proliferation genes. Underexpressed genes comprised the NF2 interacting gene SCHIP-1 and the adenomatous polyposis coli (APC)-associated gene EB1 among others. We validated the abnormal expression of six of these genes by Q-PCR. The subset of differentially expressed genes also included four underexpressed transcripts mapping to 22q12.313.3. By Q-PCR we show that one of these genes, 7 CBX7(22q13.1), was deleted in 55% of cases. Other genes mapping to cytogenetic hot spots included two overexpressed and three underexpressed genes mapping to 1q31-41 and 6q21-q24.3, respectively. These genes represent candidate genes involved in ependymoma tumorigenesis. To the authors' knowledge, this is the first time microarray analysis and Q-PCR have been linked to identify heterozygous/homozygous deletions.
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