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Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [RNA-seq]

ABSTRACT: Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [RNA-seq]

PROVIDER: PRJNA948039 | ENA |

REPOSITORIES: ENA

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Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics

Project description:Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics

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Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [DNA methylation]

Project description:Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [DNA methylation]

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Human pluripotent stem cell-derived brain tumor model uncovered embryonic stem cell signature as a key driver in atypical teratoid/rhabdoid tumor (microarray)

2019-06-20 | GSE118653 | GEO

Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-15 | GSE228103 | GEO

Recurrent atypical teratoid/rhabdoid tumors (AT/RT) reveal discrete features of progression on histology, epigenetics, copy number profiling, and transcriptomics.

Project description: Not available

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Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [RNA-seq]

Project description:Here, we investigated tumor tissue from 26 patients affected by AT/RT to identify signatures of recurrences in comparison to matched primary tumor samples. Therefore, we performed histological analysis and DNA methylation and gene expression profiling.

2023-07-15 | GSE228101 | GEO

Relapsed atypical teratoid/rhabdoid tumors (AT/RT) reveal distinct features of progression on histology, epigenetics, copy number profiling, and transcriptomics [DNA methylation]

Project description:Here, we investigated tumor tissue from 26 patients affected by AT/RT to identify signatures of recurrences in comparison to matched primary tumor samples.

2023-07-15 | GSE228091 | GEO

Natural and cryptic peptides dominate the immunopeptidome of atypical teratoid rhabdoid tumors.

Project description:Atypical teratoid/rhabdoid tumors (AT/RT) are highly aggressive CNS-tumors of infancy and early childhood. Hallmark is the surprisingly simple genomics with a truncating mutation in the SMARCB1 gene as the oncogenic driver. Nevertheless, AT/RTs are infiltrated by immune cells and even clonally expanded T-cells. However, it is unclear, what T-cells might recognize on AT/RT cells. Here, we report a comprehensive analysis of naturally presented HLA-class-I and class-II ligands on n=23 AT/RTs. MS-based analysis of the HLA-ligandome revealed 55 class-I and 139 class-II peptides from tumor-associated proteins.

2022-05-31 | PXD033935 | Pride

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.

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Human pluripotent stem cell-derived brain tumor model uncovered embryonic stem cell signature as a key driver in atypical teratoid/rhabdoid tumor (RNA-Seq)

Project description:Atypical teratoid/rhabdoid tumor (AT/RT), which harbors INI1 mutation and exhibits a characteristic histology of rhabdoid cells, has a poor prognosis because of the lack of effective treatments. Here we established human INI1-deficient pluripotent stem cells (hPSCs), which developed AT/RT formation in vivo. We revealed that the activation of ESC-like signature leads to rhabdoid phenotype in tumor by OSKM or c-MYC induction. Finally, we performed CRISPR/Cas9 knockout screening to inhibit activation of ESC-like signature in AT/RT. Our effort identified candidate genes including RAD21 that encodes a key component within the cohesin complex. Notably, chemical inhibition of HDAC8 that indirectly targets the function of cohesin with simultaneous inhibition of EZH2 efficiently suppressed the activation of ESC-like signature and inhibited the growth of AT/RT cells both in vitro and in vivo.

2019-06-20 | GSE118654 | GEO

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