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MiRNA Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

ABSTRACT: 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

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE109943 | GEO | 2019/04/15

REPOSITORIES: GEO

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Gene Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

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

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

miRNA Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

Project description:miRNA Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

| PRJNA432404 | ENA

Gene Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

Project description:Gene Expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

| PRJNA432403 | ENA

miRNA and mRNA expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

Project description:miRNA and mRNA expression data from CD133+CD15+ chordoma cells (Chordoma Cance Stem Cells) and CD133-CD15- chordoma cells

| PRJNA432398 | ENA

A novel chordoma xenograft allows in vivo drug testing and reveals the importance of NF-kB signaling in chordoma biology [SNP array]

Project description:Chordoma is a rare primary bone malignancy that arises in the skull base, spine and sacrum and originates from remnants of the notochord. These tumors are typically resistant to conventional chemotherapy, and to date there are no FDA-approved agents to treat chordoma. The lack of in vivo models of chordoma has impeded the development of new therapies for this tumor. Primary tumor from a sacral chordoma was xenografted into NOD/SCID/IL-2R Î³-null mice. The xenograft is serially transplantable and was characterized by both gene expression analysis and whole genome SNP genotyping. The NIH Chemical Genomics Center performed high-throughput screening of 2,816 compounds using two established chordoma cell lines, U-CH1 and U-CH2B. The screen yielded several compounds that showed activity and two, sunitinib and bortezomib, were tested in the xenograft. Both agents slowed the growth of the xenograft tumor. Sensitivity to an inhibitor of IÎºB, as well as inhibition of an NF-ÎºB gene expression signature demonstrated the importance of NF-ÎºB signaling for chordoma growth. This serially transplantable chordoma xenograft is thus a practical model to study chordomas and perform in vivo preclinical drug testing. The copy number and allelic balance pattern of a novel human chordoma xenograft samples was determined with Illumina BeadChips.

2013-12-22 | E-GEOD-50136 | biostudies-arrayexpress

Expression data from chordoma and notochord (microarray)

Project description:Chordoma is a rare malignant tumor thought to originate from embryonic notochord. However, no molecular comparison of chordoma and notochord has been performed to date, leaving the identities of dysregulated pathways unclear. Absence of a molecular description of a control tissue clouds our understanding of chordoma. Thus, we conducted an unbiased comparison of chordoma and notochord using gene expression profiling to clarify chordoma’s tissue of origin and identify novel drug targets

2023-02-07 | GSE224776 | GEO

Expression data from chordoma and notochord (RNA-Seq)

2023-02-07 | GSE205457 | GEO

A novel chordoma xenograft allows in vivo drug testing and reveals the importance of NF-kB signaling in chordoma biology [expression array]

Project description:Chordoma is a rare primary bone malignancy that arises in the skull base, spine and sacrum and originates from remnants of the notochord. These tumors are typically resistant to conventional chemotherapy, and to date there are no FDA-approved agents to treat chordoma. The lack of in vivo models of chordoma has impeded the development of new therapies for this tumor. Primary tumor from a sacral chordoma was xenografted into NOD/SCID/IL-2R γ-null mice. The xenograft is serially transplantable and was characterized by both gene expression analysis and whole genome SNP genotyping. The NIH Chemical Genomics Center performed high-throughput screening of 2,816 compounds using two established chordoma cell lines, U-CH1 and U-CH2B. The screen yielded several compounds that showed activity and two, sunitinib and bortezomib, were tested in the xenograft. Both agents slowed the growth of the xenograft tumor. Sensitivity to an inhibitor of IκB, as well as inhibition of an NF-κB gene expression signature demonstrated the importance of NF-κB signaling for chordoma growth. This serially transplantable chordoma xenograft is thus a practical model to study chordomas and perform in vivo preclinical drug testing. Total five microarray experiments were conducted, two of which are for chordoma xenograft sammples and three for chrodoma primary tumor. RNA extracted from xenograft samples and from chordomas was hybridized to Illumina arrays.

2013-12-22 | E-GEOD-50135 | biostudies-arrayexpress

A novel chordoma xenograft allows in vivo drug testing and reveals the importance of NF-kB signaling in chordoma biology [expression array]

Project description:Chordoma is a rare primary bone malignancy that arises in the skull base, spine and sacrum and originates from remnants of the notochord. These tumors are typically resistant to conventional chemotherapy, and to date there are no FDA-approved agents to treat chordoma. The lack of in vivo models of chordoma has impeded the development of new therapies for this tumor. Primary tumor from a sacral chordoma was xenografted into NOD/SCID/IL-2R γ-null mice. The xenograft is serially transplantable and was characterized by both gene expression analysis and whole genome SNP genotyping. The NIH Chemical Genomics Center performed high-throughput screening of 2,816 compounds using two established chordoma cell lines, U-CH1 and U-CH2B. The screen yielded several compounds that showed activity and two, sunitinib and bortezomib, were tested in the xenograft. Both agents slowed the growth of the xenograft tumor. Sensitivity to an inhibitor of IκB, as well as inhibition of an NF-κB gene expression signature demonstrated the importance of NF-κB signaling for chordoma growth. This serially transplantable chordoma xenograft is thus a practical model to study chordomas and perform in vivo preclinical drug testing.

2013-12-22 | GSE50135 | GEO

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