Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression data from ETMR cell line BT183

ABSTRACT: Gene expression data from this ETMR cell line was compared with gene expression data from primary ETMR tumors to search for potential drug targets in ETMR tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94985 | GEO | 2020/02/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome wide methylation profliling of ETMR tumours.

Project description:Genome wide DNA methylation profiling of normal, ETMR and PNET tumours Bisulphite converted DNA from 12 ETMR, 28 PNET and 34 control samples hybridised to the Illumina 450k Human Methylation Beadchip Please note that three of the 12 EMTR samples are tumor, cell line and xenograft sample derived from a single patient. Thus, there are 10 ETMR patients, 12 samples.

2013-11-21 | E-GEOD-52556 | biostudies-arrayexpress

Integrated proteomics spotlight the proteasome as a pervasive therapeutic vulnerability in Embryonal Tumors with Multilayered Rosettes (ETMR)

Project description:Embryonal tumors with multilayered rosettes (ETMR) are rare malignant embryonal brain tumors. The prognosis of ETMR is poor and novel therapeutic approaches are desperately needed. Comprehension of ETMR tumor biology is based on only few previous molecular studies, which mainly relied on the analyses of nucleic acids. In this study, we explored integrated ETMR proteomics with the aim to identify novel therapeutic vulnerabilities in these deadly tumors. Using mass spectrometry, proteome data were acquired from FFPE tissue of 40 embryonal brain tumors (16 ETMR, 9 atypical teratoid/rhabdoid tumors (AT/RT), 15 medulloblastomas (MB)) and integrated with case-matched global DNA methylation data, publicly available transcriptome data, and proteome data of further pediatric brain tumors. Proteome-based cluster analyses grouped ETMR samples according to histomorphology, separating neuropil-rich tumors with neuronal signatures from primitive tumors with signatures relating to stemness and chromosome organization. Microdissection analyses highlighted the close relationship of ETMR histomorphology and proteome profiles, regardless of intra- or intertumoral comparisons. Integrated proteomics showcased that ETMR harbor proteasome regulatory proteins in abundancy, implicating their strong dependency on the proteasome machinery to safeguard proteostasis. Respectively, in vitro cell culture viability assays using embryonal brain tumor cell lines BT183 (ETMR), BT16 (AT/RT), and D283 (MB) highlighted that ETMR cells were highly vulnerable towards treatment with the CNS penetrant proteasome inhibitor Marizomib. In summary, histomorphology stipulates the proteome signatures of ETMR. Pervasive and histomorphology-independent abundancy of proteasome regulatory proteins in ETMR indicates a strong proteasome dependency throughout these tumors. As validated in cell culture experiments, proteasome inhibition poses a promising therapeutic option in ETMR.

2024-01-08 | PXD045268 | Pride

Methylation profiling of preclinical ETMR models

Project description:Methylation profiles of preclinical ETMR models were generated and compared to reference primary human tumors to determine the molecular fidelity of the preclinical model systems.

2018-02-14 | GSE94987 | GEO

ETMR-like infantile cerebellar embryonal tumors in the extended morphologic spectrum of DICER1-related tumors

Project description:Description of two cases of ETMR-like cerebellar tumors with DICER1 mutations

2018-09-19 | GSE120122 | GEO

Genome wide methylation profliling of ETMR tumours.

Project description:Genome wide DNA methylation profiling of normal, ETMR and PNET tumours

2013-11-21 | GSE52556 | GEO

The Molecular Landscape of ETMR at Diagnosis and Relapse [methylation]

Project description:ETMRs are aggressive pediatric embryonal brain tumors with universally dismal outcome. We collected 193 ETMR samples and an additional 23 matched relapses to investigate the genomic landscape of this distinct entity. We found that patients having tumors without C19MC amplification, the proposed driver, frequently harbor DICER1 germline mutations or other miRNA-related aberrations such as somatic miR-17-92 miRNA cluster amplifications. Despite these distinct genetic aberrations, no molecular subgrouping was observed. Whole-genome sequencing revealed an overall low recurrence of SNVs, but prevalent R-loop-associated chromosomal instability, of which we show that this can be induced by loss of DICER1 function. Comparing primary tumors and matched relapses revealed a strong conservation of SVs but low conservation of SNVs. Moreover, many newly acquired SNVs are associated to a new cisplatin treatment related mutational signature. Finally, we show that targeting R-loops with topoisomerase and PARP inhibitors might be an effective treatment strategy for this deadly disease.

2019-08-26 | GSE122038 | GEO

The Molecular Landscape of ETMR at Diagnosis and Relapse [gene expression]

2019-08-26 | GSE122077 | GEO