EGAS00001000895-sc-20150128 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001001239 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAD00001001238 | EGA
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAS00001000895 | EGA
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAS00001000892 | EGA
Project description:This cohort is an extension of our previous dataset (Spiers et al) containing DNA methylation profiled with the EPIC array on an additional 40 human fetal brain samples. Please note that these samples are from the same cohort as GSE58885.
2021-06-30 | GSE157908 | GEO
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
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
Project description:Chordoma is a rare, resistant bone tumor thought to be arised from remnants of embryonic notochord. Cancer stem cells (CSCs) are associated with tumorigenesis, recurrence and resistance in cancers. Here, we used miRNA and mRNA transcriptome analysis to discover novel genes and networks in chordoma CSCs
2019-04-15 | GSE109943 | GEO
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains genome-wide binding profile of the factor sc from E0-12 generated by ChIP and analyzed on Illumina Genome Analyzer. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf A validated dataset is comprised of three biological replicates for ChIP-chip experiments and two replicates for ChIP-seq and meet the modENCODE quality standards. The control sample is the chromatin Input used for ChIP. Most factors binding profiles are generated by using specific antibodies for the protein of interest. However, some factors have been tagged by GFP in a transgenic line. In that case, ChIP is generated using an anti-GFP antibody. This submission represents the ChIP-seq component of the study.
2011-12-16 | E-GEOD-34347 | biostudies-arrayexpress
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains genome-wide binding profile of the factor sc from E0-8 generated by ChIP and analyzed on Illumina Genome Analyzer. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf A validated dataset is comprised of three biological replicates for ChIP-chip experiments and two replicates for ChIP-seq and meet the modENCODE quality standards. The control sample is the chromatin Input used for ChIP. Most factors binding profiles are generated by using specific antibodies for the protein of interest. However, some factors have been tagged by GFP in a transgenic line. In that case, ChIP is generated using an anti-GFP antibody. This submission represents the ChIP-seq component of the study.
2011-12-28 | E-GEOD-34712 | biostudies-arrayexpress
Project description:Chordoma is a rare, resistant bone tumor thought to be arised from remnants of embryonic notochord. Cancer stem cells (CSCs) are associated with tumorigenesis, recurrence and resistance in cancers. Here, we used miRNA and mRNA transcriptome analysis to discover novel genes and networks in chordoma Cancer Stem Cells
2020-01-01 | GSE109944 | GEO