ArticlePediatric blood & cancer2013
Pediatric rhabdoid tumors of kidney and brain show many differences in gene expression but share dysregulation of cell cycle and epigenetic effector genes.
Article in Pediatric blood & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 52 citations in OpenAlex.
- Identification and validation of exosome-related biomarkers in pediatric glioblastoma.Discover oncology · 2026Article
- Identification and validation of feature genes using a ferroptosis-informed analytical framework in medulloblastoma.Frontiers in pediatrics · 2026Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- TheBiomolecules · 2025Review
- Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumors.Life science alliance · 2024Article
- Targeting of RRM2 suppresses DNA damage response and activates apoptosis in atypical teratoid rhabdoid tumor.Journal of experimental & clinical cancer research : CR · 2023Article
- Comprehensive Analysis of Tumor Microenvironment Reveals Prognostic ceRNA Network Related to Immune Infiltration in Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Identification ofFrontiers in oncology · 2023Article
- Identification of PBK as a hub gene and potential therapeutic target for medulloblastoma.Oncology reports · 2022Article
- Targeting the TP53/MDM2 axis enhances radiation sensitivity in atypical teratoid rhabdoid tumors.International journal of oncology · 2022Article
- TOP2A correlates with poor prognosis and affects radioresistance of medulloblastoma.Frontiers in oncology · 2022Article
- Current and Emerging Therapeutic Approaches for Extracranial Malignant Rhabdoid Tumors.Cancer management and research · 2022Review
- Maternal embryonal leucine zipper kinase immunoreactivity in atypical teratoid/rhabdoid tumors: a study of 50 cases.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- Differential gene expression-based connectivity mapping identified novel drug candidate and improved Temozolomide efficacy for Glioblastoma.Journal of experimental & clinical cancer research : CR · 2021Article
- TheFrontiers in molecular neuroscience · 2021Article
- Identification of Core Genes and Pathways in Medulloblastoma by Integrated Bioinformatics Analysis.Journal of molecular neuroscience : MN · 2020Article
- Age and DNA methylation subgroup as potential independent risk factors for treatment stratification in children with atypical teratoid/rhabdoid tumors.Neuro-oncology · 2020Article
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Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundRhabdoid tumors (RTs) are aggressive tumors of early childhood that occur most often in brain (AT/RTs) or kidney (KRTs). Regardless of location, they are characterized by loss of functional SMARCB1 protein, a component of the SWI/SNF chromatin remodeling complex. The aim of this study was to determine genes and biological process dysregulated in common to both AT/RTs and KRTs. PROCEDURE: Gene expression for AT/RTs was compared to that of other brain tumors and normal brain using microarray data from our lab. Similar analysis was performed for KRTs and other kidney tumors and normal kidney using data from GEO. Dysregulated genes common to both analyses were analyzed for functional significance.
resultsUnsupervised hierarchical clustering of RTs identified three major subsets: two comprised of AT/RTs, and one of KRTs. Compared to other tumors, 1,187, 663, and 539 genes were dysregulated in each subset, respectively. Only 14 dysregulated genes were common to all three subsets. Compared to normal tissue, 5,209, 4,275, and 2,841 genes were dysregulated in each subset, with an overlap of 610 dysregulated genes. Among these genes, processes associated with cell proliferation, MYC activation, and epigenetic dysregulation were common to all three RT subsets.
conclusionsThe low overlap of dysregulated genes in AT/RTs and KRTs suggests that factors in addition to SMARCB1 loss play a role in determining subsequent gene expression. Drugs which target cell cycle or epigenetic genes may be useful in all RTs. Additionally, targeted therapies tailored to specific RT subset molecular profiles should be considered.
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Registered trials
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