Roussel-ATRT-TM WXS - samples
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ABSTRACT:
PROVIDER: EGAD00001009164 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:WGS files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00001009163 | EGA
Project description:RNASeq files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00001009302 | EGA
Project description:Methylation files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00010002357 | EGA
Project description:Additional WXS files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00001010265 | EGA
Project description:Additional WGS files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00001010264 | EGA
Project description:Additional Methylation files for Roussel-ATRT-TM paper titled "Atypical teratoid/ rhabdoid tumoroids reveal subgroup-specific drug vulnerabilities"
| EGAD00010002495 | EGA
Project description:Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tumors in infants. Although the prognosis of ATRT patients is poor, some patients respond favorably to current treatments, suggesting molecular inter-tumor heterogeneity. To investigate this further, we genetically and epigenetically analyzed a large series of human ATRTs. Three distinct molecular subgroups of ATRTs, associated with differences in demographics, tumor location, and type of SMARCB1 alterations, were identified. Whole-genome DNA and RNA sequencing found no recurrent mutations in addition to SMARCB1 that would explain the differences between subgroups. Whole-genome bisulfite sequencing and H3K27Ac chromatin-immunoprecipitation sequencing of primary tumors, however, revealed clear differences, leading to the identification of subgroup-specific regulatory networks and potential therapeutic targets. 49 ATRT samples were selected for RNA extraction and hybridization on Affymetrix Affymetrix Human Genome U133 Plus 2.0 Arrays. ---------------------------------------- This submission consists of the expression data for 49 of 170 samples only
2016-03-02 | E-GEOD-70678 | biostudies-arrayexpress
Project description:Clinical and molecular risk factors were analyzed in a large cohort of patients with Atypical Teratoid Rhabdoid Tumors (ATRT) recruited to the European Rhabdoid Regsitry (EU-RHAB) and data were validated in a second independent cohort of ATRT patients.
2020-01-31 | GSE141039 | GEO
Project description:The samples deposited here are part of the ATRT consensus cohort as published in Ho et al. ("Molecular subgrouping of Atypical Teratoid/Rhabdoid Tumors (ATRT) - a reinvestigation and current consensus") and have so far not been included in any publication.
2020-01-31 | GSE141363 | GEO
Project description:Atypical teratoid rhabdoid tumor (ATRT) is a highly aggressive brain tumor of childhood with a poor overall survival. The salient molecular feature of ATRT is the loss of SMARCB1 which results in epigenetic dysregulation of the genome. SMARCB1 loss affects lineage commitment and differentiation by controlling gene expression. We hypothesized that additional epigenetic factors co-operate with SMARCB1 loss to control cell self-renewal and drive ATRT. We identified SIRT2 as a primary dependency in ATRT. Using a combination of RNA-seq, CUT&RUN and single RNA sequencing in model systems ATRT, we observed genome-wide reorganization of active chromatin and significantly changes in genes expression in ATRT cells with genetic (with shRNA) or chemical (with Tenovin or Thiomyristoyl (TM)) SIRT2 deactivation. Single-cell RNA transcriptome analysis of xenograft tumors revealed the elimination of tumor cells expressing stem cell genes and expansion of tumor cells expressing differentiated genes in vivo. Furthermore, SIRT2 inhibition induced apoptosis, decreased tumor growth and prolonged survival in orthotopic xenograft models. In summary we demonstrated that SIRT2 inhibition is a molecular vulnerability in SMARCB1-deleted tumors with therapeutic potential.
2025-06-16 | GSE278558 | GEO