Chordoma Extension known cancer genes
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001000895 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAS00001000892 | EGA
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAD00001001239 | EGA
Project description:Extension analysis to pursue candidate genes of interest in chordoma
| EGAD00001001238 | EGA
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: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
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: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
Project description:Chromatin profiling of chordoma collected by the Broad chordoma target discovery project
2015-07-11 | GSE70771 | 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:Identifying the spectrum of genes required for cancer cell survival can reveal essential cancer circuitry and therapeutic targets, but such a map remains incomplete for many cancer types. We apply genome-scale CRISPR-Cas9 loss-of-function screens to map the landscape of selectively essential genes in chordoma, a bone cancer with few validated targets. This approach confirms a known chordoma dependency, TBXT (T; brachyury), and identifies a range of additional dependencies, including PTPN11, ADAR, PRKRA, LUC7L2, SRRM2, SLC2A1, SLC7A5, FANCM, and THAP1. CDK6, SOX9, and EGFR, genes previously implicated in chordoma biology, are also recovered. We find genomic and transcriptomic features that predict specific dependencies, including interferon-stimulated gene expression, which correlates with ADAR dependence and is elevated in chordoma. Validating the therapeutic relevance of dependencies, small-molecule inhibitors of SHP2, encoded by PTPN11, have potent preclinical efficacy against chordoma. Our results generate an emerging map of chordoma dependencies to enable biological and therapeutic hypotheses.
2023-03-09 | GSE226734 | GEO