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Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [I]

ABSTRACT: CRISPR/Cas9 knockout screens were performed to identify genetic dependencies of ATRT cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230742 | GEO | 2024/10/01

REPOSITORIES: GEO

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Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [II]

Project description:CRISPR/Cas9 knockout screens were performed to identify genetic dependencies of ATRT cell lines.

2024-10-01 | GSE231286 | GEO

Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [III]

Project description:CRISPR/Cas9 knockout screens were performed to identify genetic dependencies of ATRT cell lines. This submission covers methylation analyses of human ATRT cell lines as assessed by the Illumina Infinium HumanMethylation850 BeadChip array.

2024-10-01 | GSE231533 | GEO

Investigation of genetic dependencies in atypical teratoid rhabdoid tumors

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

2024-10-01 | GSE231287 | GEO

Investigation of genetic dependencies in atypical teratoid rhabdoid tumors

Project description:Investigation of genetic dependencies in atypical teratoid rhabdoid tumors

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Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [II]

Project description:Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [II]

| PRJNA963052 | ENA

Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [I]

Project description:Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [I]

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Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [III]

Project description:Investigation of genetic dependencies in atypical teratoid rhabdoid tumors (ATRTs) [III]

| PRJNA966246 | ENA

The genomic and epigenomic landscape of atypical teratoid rhabdoid tumors

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.

2016-03-02 | GSE70460 | GEO

SMARCB1 loss induces druggable cyclin D1 deficiency via upregulation of MIR17HG in atypical teratoid rhabdoid tumors

Project description:Atypical teratoid rhabdoid tumor (ATRT) is a fatal pediatric malignancy of the central neural system lacking effective treatment options. It belongs to rhabdoid tumor family usually caused by biallelic inactivation of SMARCB1, encoding a key subunit of SWI/SNF chromatin remodelling complexes. Previous studies proposed that SMARCB1 loss drives rhabdoid tumor by promoting cell cycle through activating transcription of cyclin D1 while suppressing p16. However, low cyclin D1 protein expression is observed in most ATRT patient tumors. The underlying mechanism and therapeutic implication of this molecular trait remain unknown. Here, we show that SMARCB1 loss in ATRT leads to the reduction of cyclin D1 expression by upregulating MIR17HG, a microRNA (miRNA) cluster known to generate multiple miRNAs targeting CCND1. Furthermore, we find that this cyclin D1 deficiency in ATRT results in marked in vitro and in vivo sensitivity to the CDK4/6 inhibitor palbociclib as a single agent. Our study identifies a novel genetic interaction between SMARCB1 and MIR17HG in regulating cyclin D1 in ATRT and suggests a rationale to treat ATRT patients with FDA-approved CDK4/6 inhibitors.

2020-06-08 | GSE147851 | GEO

Wnt pathway in atypical teratoid rhabdoid tumors.

Project description:Atypical teratoid rhabdoid tumor (ATRT) is an aggressive pediatric brain tumor with limited therapeutic options. The hypothesis for this study was that the Wnt pathway triggered by the Wnt5B ligand plays an important role in ATRT biology. To address this hypothesis, the role of WNT5B and other Wnt pathway genes was analyzed in ATRT tissues and ATRT primary cell lines.Transcriptome-sequencing analyses were performed using nanoString platforms, immunohistochemistry, Western blotting, quantitative reverse transcriptase PCR, immunoprecipitation, short interference RNA studies, cell viability studies, and drug dose response (DDR) assays.Our transcriptome-sequencing results of Wnt pathway genes from ATRT tissues and cell lines indicated that the WNT5B gene is significantly upregulated in ATRT samples compared with nontumor brain samples. These results also indicated a differential expression of both canonical and noncanonical Wnt genes. Imunoprecipitation studies indicated that Wnt5B binds to Frizzled1 and Ryk receptors. Inhibition of WNT5B by short interference RNA decreased the expression of FRIZZLED1 and RYK. Cell viability studies a indicated significant decrease in cell viability by inhibiting Frizzled1 receptor. DDR assays showed promising results with some inhibitors.These promising therapeutic options will be studied further before starting a translational clinical trial. The success of these options will improve care for these patients.

| S-EPMC4483069 | biostudies-literature

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