Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrative analyses of rhabdoid tumors across all anatomical sites reveal subgroups with possible immune modulation through epigenetic dysregulation

ABSTRACT: Extra-cranial malignant rhabdoid tumors (MRTs) and cranial atypical teratoid RTs (ATRTs) are pediatric cancers driven by SMARCB1 loss. To understand biological relationships between MRTs and ATRTs, we performed integrative data analyses of 140 MRTs and 161 ATRTs, and detected features conserved between MRTs and the MYC subgroup of ATRTs, including global DNA hypomethylation and over-expression of HOX and mesenchymal development genes, thereby distinguishing them from other ATRT subgroups that exhibit neural-like features. Our analyses revealed five DNA-methylation subgroups associated with distinct anatomical sites, SMARCB1 alteration patterns, and distinct gene-expression and enhancer profiles. We also report on RT subgroups with expression patterns indicative of both increased immune infiltration and expression of immune checkpoint genes, which were confirmed using immunohistochemical techniques.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123601 | GEO | 2019/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression data from ATRT tumor samples

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

The genomic and epigenomic landscape of atypical teratoid rhabdoid tumors

2016-03-02 | GSE70460 | GEO

Gene expression data from ATRT tumor samples

2016-03-02 | GSE70678 | GEO

RNA sequencing data from primary atypical teratoid rhabdoid tumor (ATRT) samples

Project description:Atypical teratoid/rhabdoid tumors (ATRTs) are very aggressive childhood malignancies of the central nervous system. The underlying genetic cause are inactivating bi-allelic mutations in SMARCB1 or (rarely) in SMARCA4. The purpose of this study was to compare the transcriptomes of ATRTs with SMARCA4 mutations to those carrying SMARCB1 mutations.

2020-12-18 | GSE160748 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [DNAmeth_EPICarray]

Project description:Atypical teratoid rhabdoid tumors (ATRT) are divided into MYC, TYR and SHH subgroups, suggesting diverse lineages of origin. Here, we investigate the imaging of human ATRT at diagnosisand the precise anatomic origin of brain tumors in the Rosa26; Cre-ERT2::Smarcb1flox/flox model. This cross-species analysis points to an extra-cerebral origin for MYC tumors. Additionally, we clearly distinguish SHH ATRT emerging from the cerebellar anterior lobe (CAL) from those emerging from the basal ganglia (BG) and intra-ventricular (IV) regions. Molecular characteristics point to the midbrain-hindbrain boundary as the origin of CAL SHH ATRT, and to the ganglionic eminence as the origin of BG/IV SHH ATRT. Single-cell RNA sequencing on SHH ATRT supports these hypotheses. Trajectory analyses suggest that SMARCB1 loss induces a de-differentiation process mediated by repressors of the neuronal program such as REST, ID and the NOTCH pathway.

2023-09-20 | GSE242089 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [bulkRNAseq_primaryATRT]

2023-09-20 | GSE241831 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [scRNAseq_ATRT_CAL]

2023-09-20 | GSE241737 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [scRNAseq_mouseRT_R26SHH]

2023-09-20 | GSE241736 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [bulkRNAseq_mouseRT_R26]

2023-09-20 | GSE241734 | GEO

Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups [bulkRNAseq_ATRT_cellLines]

2023-09-20 | GSE241733 | GEO