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Comprehensive analysis of the (epi)genome of pediatric atypical teratoid/rhabdoid tumours (AT/RTs)

Whole exome sequencing of atypical teratoid /rhabdoid tumors (AT/RTs) revealed recurrent mutations only in SMARCB1, a gene involved in chromatin remodeling. However, preliminary data from our lab using gene expression and DNA methylation arrays shows that there are three distinct molecular subgroups of AT/RTs, suggesting that other molecular alterations underlying the development of these aggressive pediatric brain tumors must be found outside the coding genome or at the epigenomic level. Identification of these (epi)genomic alterations, which we intend to address in this project, may lead to novel treatment strategies for these tumors and reveal options for meaningful patient stratification.

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID Description Technology Samples
EGAD00001001444 Illumina HiSeq 2000 Illumina HiSeq 2500 55
EGAD00001002135 Illumina HiSeq 2000 Illumina HiSeq 2500 15
EGAD00001002136 Illumina HiSeq 2000 25
EGAD00001002137 Illumina HiSeq 2000 Illumina HiSeq 2500 15
EGAD00001002138 Illumina HiSeq 2000 36
EGAD00001003408 Illumina HiSeq 2000 19
Publications Citations
Comprehensive Analysis of Chromatin States in Atypical Teratoid/Rhabdoid Tumor Identifies Diverging Roles for SWI/SNF and Polycomb in Gene Regulation.
Cancer Cell 35: 2019 95-110.e8
Identification and Analyses of Extra-Cranial and Cranial Rhabdoid Tumor Molecular Subgroups Reveal Tumors with Cytotoxic T Cell Infiltration.
Cell Rep 29: 2019 2338-2354.e7
Pilocytic astrocytoma demethylation and transcriptional landscapes link bZIP transcription factors to immune response.
Neuro Oncol 22: 2020 1327-1338
Locoregionally administered B7-H3-targeted CAR T cells for treatment of atypical teratoid/rhabdoid tumors.
Nat Med 26: 2020 712-719