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Affymetrix SNP 6.0 array data for chordoma samples

ABSTRACT: Chordomas are rare, low to intermediate grade malignant bone tumors of the axial skeleton, believed to originate from the notochord. Treatment options are limited and mainly restricted to surgical excision, as chordomas have been proven to be largely resistant to conventional ionizing radiation and chemotherapy. Therefore a new cell line was established. The cell line has been characterized by immunohistochemistry,western blot and karyotyping using cobra fish technology. Copy number variations (CNV) and loss-of heterozygosity (LOH) from fibroblasts, tumor tissue, low and high cell line passage was evaluted by using Affymetrix 6.0SNP Arrays. DNA isolated from the patients MNCs was used as control. The cell line MUG-Chor1 is highly similar to genetic profiles of chordomas and provides therefore a powerful tool for further investigations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25720 | GEO | 2012/07/12

SECONDARY ACCESSION(S): PRJNA133847

REPOSITORIES: GEO

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Affymetrix SNP 6.0 array data for chordoma samples

Project description:Chordomas are rare, low to intermediate grade malignant bone tumors of the axial skeleton, believed to originate from the notochord. Treatment options are limited and mainly restricted to surgical excision, as chordomas have been proven to be largely resistant to conventional ionizing radiation and chemotherapy. Therefore a new cell line was established. The cell line has been characterized by immunohistochemistry,western blot and karyotyping using cobra fish technology. Copy number variations (CNV) and loss-of heterozygosity (LOH) from fibroblasts, tumor tissue, low and high cell line passage was evaluted by using Affymetrix 6.0SNP Arrays. DNA isolated from the patients MNCs was used as control. The cell line MUG-Chor1 is highly similar to genetic profiles of chordomas and provides therefore a powerful tool for further investigations. Affymetrix SNP 6.0 arrays were performed according to the manufacturer's directions on DNA extracted from cryo material or cell lines. Copy number analysis of Affymetrix SNP 6.0 arrays was performed for 4 samples. 60 samples from HapMap database were used as references for copy number inference.

2012-07-11 | E-GEOD-25720 | 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. 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

Multimodal assessment of chordoma immunity reveals distinct immune contextures

Project description:Chordomas are cancers from the axial skeleton presenting immunological hallmarks of unknown significance. In recent years, some clinical trials demonstrated that chordomas can respond to immunotherapy. We present a comprehensive characterisation of immunological features of 76 chordomas through application of a multimodal approach comprising transcriptional profiling, multidimensional immunophenotyping and TCR profiling. Chordomas generally presented an immune “hot” microenvironment in comparison to other sarcomas, as indicated by the immunologic constant of rejection transcriptional signature. We identified two distinct groups of chordomas based on T cell infiltration. The highly infiltrated group was further characterised by high dendritic cell infiltration and the presence of multicellular immune aggregates in tumours, whereas low T cell infiltration was associated with lower overall cell densities of immune and stromal cells. Interestingly, patients with higher T cell infiltration displayed a more pronounced clonal enrichment of the T cell receptor repertoire compared to those with low T cell counts. Furthermore, we observed that the majority of chordomas maintained HLA class I expression. Our findings shed light on the natural immunity against chordomas. Understanding their immune landscape could guide the development and application of immunotherapies in a tailored manner, ultimately leading to an improved clinical outcome for chordoma patients.

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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

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2014-03-29 | E-GEOD-56183 | 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

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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.

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