Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Establishment of a tumour progression model in chordoma

ABSTRACT: mRNA profiling of three novel chordoma cell lines out of the same patient. The gene expression profiles of the primary tumour derived cell line U-CH17P was compared to the gene expression profiles of the metastases derived cell lines U-CH17S and U-CH17M in order to spot differently expressed genes, that are involved in the formation of metastases in chordoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98021 | GEO | 2017/10/02

SECONDARY ACCESSION(S): PRJNA383679

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

miRNA profiling of sacral chordoma and nucleus pulposus cells

Project description:Next-generation RNA sequencing (NGS) was used for the combinatorial analysis of mRNA-miRNA gene expression profiles in sacral chordoma and nucleus pulposus samples, and to predict miRNA-mRNA regulatory networks with altered activity in chordoma. We identified a gene set including key regulators of the Hippo pathway, which is targeted by differently expressed miRNAs, and validated their altered expression by RT-qPCR. These newly identified miRNA/RNA interactions are predicted to have a role in the self-renewal process of chordoma stem cells, which might sustain the high rate of recurrence for this tumor.

2022-07-28 | GSE209695 | GEO

Chordoma ATAC-Seq

Project description:Chromatin profiling of chordoma collected by the Broad chordoma target discovery project paired end ATAC-Seq profiling in the UCH2 and MUGCHOR chordoma cell lines

2015-07-11 | E-GEOD-70771 | biostudies-arrayexpress

Affect of Interferon Gamma on Chordoma Cells

Project description:IFN-g-induced gene expression profiles of UM-Chor1 cells were assessed by microarray analysis Chordoma is a rare bone tumor derived from notochord, which has shown to be resistant to conventional therapy, including chemotherapy and radiotherapy. Immunotherapy has the potential to be effective in cancers with resistance to conventional therapy. Checkpoint inhibition, including Programmed cell Death 1 (PD-1)/Programmed cell Death protein 1 (PD-L1) blockade has shown great promise in treating diverse cancers. The purpose of this study was to investigate the potential of anti-PD-L1 antibody therapy for chordoma. To this end, using 4 chordoma cell lines, we examined the expression of PD-L1 and performed in vitro NK cells killing assay for antibody-dependent cell-mediated cytotoxicity (ADCC) activity mediated by the anti-PD-L1 antibody, avelumab. Here, the expression of PD-L1 was markedly upregulated by IFN-g in all 4 chordoma cell lines, which resulted in increasing the sensitivity to ADCC. Next, to model a patient that received a tumor-antigen specific vaccine, chordoma cells were co-incubated with brachyury specific CD8+ T cells, culminating in significant upregulation of PD-L1 on the tumor cells mediated by CD8+ T cells IFN-g production. The functional consequence was the sensitivity of chordoma cells to ADCC mediated by avelumab. Finally, residential cancer stem cell subpopulations of chordoma cells were killed by avelumab-mediated ADCC to the same degree as non-cancer stem cell populations. Our findings show the potential of avelumab therapy in chordoma; a) alone, to enable endogenous NK cells to kill chordoma cells via ADCC, or b) in conjunction with T cells immunotherapy such a vaccine, to exploit enhanced NK cell killing of chordoma cells via ADCC.

2017-01-01 | GSE77732 | GEO

Chordoma Cell Lines Characterization

Project description:mRNA Expression of established chordoma cell lines for characterization.

2015-05-05 | GSE68497 | GEO

Human skull base chordoma LC-MSMS

Project description:The prognostic factors of skull base chordoma associated with outcomes of patients after surgical resection remain poorly defined. This project aimed to identify a novel prognostic factor for patients with skull base chordoma. Using a proteomics approach, we screened tumor biomarkersthat upregulated in the rapid-recurrence group of chordoma, narrowed down by bioinformatics analysis, and finally potential biomarker was chosen for validation by immunohistochemistry using tissue microarray.

2021-11-03 | PXD025894 | Pride

Chordoma Cell Lines Characterization

Project description:mRNA Expression of established chordoma cell lines for characterization. Comparative analysis

2015-05-05 | E-GEOD-68497 | biostudies-arrayexpress

Characterization of chordoma cell lines derived from the clivus region

Project description:mRNA profiling of three clival chordoma cell lines. The expression profiles were compared to previously published expression profiles of sacral chodomas (GEO accession number: GSE68497) to determine whether there are differences in expression that indicate stricing differences on molecular grounds.

2017-04-18 | GSE95084 | GEO

Characterization of a clival chordoma xenograft model reveals inherent tumor genomic instability

Project description:Patient-derived xenografts retain the genotype of the parent tumors more readily than tumor cells maintained in culture. The two reported clival chordoma xenografts are derived from recurrent tumors after radiation. In order to study the genetics of clival chordoma in the absence of prior radiation we sought to establish a patient-derived xenograft at primary resection of a clival chordoma.

2017-08-31 | GSE103342 | GEO

Receptor Tyrosine Kinase pathway activation is sufficient to trigger chordoma in zebrafish

Project description:Oncogenic transformation of individual cell fates by developmental signaling cascades and transcription factors triggers diverse cancer types. Chordoma is a rare, aggressive tumor arising from transformed notochord remnants. Various potentially oncogenic factors have been found deregulated in chordoma and its metastases, yet clear causation remains uncertain. In particular, expression of the notochord-controlling transcription factor Brachyury is hypothesized as key molecular driver in chordoma formation, yet an in vivo model to causally test its oncogenic potential in the notochord is missing. Here, we apply a zebrafish model of chordoma onset to identify the notochord-transforming potential of tumor-implicated candidate genes in vivo. We find that overexpression of human and zebrafish Brachyury, including a version with augmented transcriptional activity, is insufficient to initiate notochord hyperplasia in vivo. In contrast, the repeatedly chordoma-implicated receptor tyrosine kinase (RTK) genes EGFR and KDR/VEGFR2 are sufficient to transform developmental notochord cells, akin to direct activation of Ras. Analysis of transcriptome and sub-cellular organization from transformed notochords suggests that aberrant activation of RTK/Ras signaling attenuates processes required for the differentiation of notochord cells. Taken together, our results provide first in vivo indication for a lack of tumor-initiating potential of Brachyury expression in the notochord, and suggest activated RTK signaling as potent hyperplasia-initiating event in chordoma.

2018-12-01 | E-MTAB-7349 | biostudies-arrayexpress