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Expression data from DTL silenced-Ewing Sarcoma's cell lines along with their controls

ABSTRACT: The 1q gain is related to poor survival, and to a profile of cell cycle deregulation in Ewing's Sarcoma (ES). Tumor samples with 1q gain overexpress the gene DTL. We have silenced DTL in three ES cell lines in order to compare the differential expression pattern produced with the differential expression pattern which characterizes 1q gained-tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20357 | GEO | 2011/08/01

SECONDARY ACCESSION(S): PRJNA129835

REPOSITORIES: GEO

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Expression data from DTL silenced-Ewing Sarcoma's cell lines along with their controls

Project description:The 1q gain is related to poor survival, and to a profile of cell cycle deregulation in Ewing's Sarcoma (ES). Tumor samples with 1q gain overexpress the gene DTL. We have silenced DTL in three ES cell lines in order to compare the differential expression pattern produced with the differential expression pattern which characterizes 1q gained-tumors. We silenced DTL in three ES cell lines with two different shRNA constructions by means of lentiviral transduction. pLKO.1-non-targeting control was transduced in the control samples. RNA was extracted and hybridized with Affymetrix expression microarrays.

2011-07-31 | E-GEOD-20357 | biostudies-arrayexpress

Project description:1q gain clinical impact in Ewing's Sarcoma: role of DTL

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Protein expression in isogenic cancer cell line models of 1q aneuploidy

Project description:Investigating differential protein expression between 1q trisomy and 1q disomy cancer cell lines in isogenic backgrounds

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Transcription profiling of human Ewing's sarcoma tumor samples and cell lines

Project description:Comparison of expression profiling from Ewing's sarcoma tumor specimen to Ewing's sarcoma cell lines

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Detection of Early Prognostic Biomarkers for Metastasis of Ewing’s Sarcoma in Pediatric Patients

Project description:Ewing’s sarcoma (ES) is a highly aggressive bone tumor, and the second most prevalent pediatric bone malignancy. The presence of metastasis at diagnosis decreases the three-year survival rate to 20% and contributes to diminished prognosis. Researches are indispensable for the early characterization of the disease and prediction of metastatic-prone patients, through biomarkers identification. Moreover, there is currently no available data on ES utilizing non-biopsy samples, such as plasma. This study utilizes a proteomic analysis of Ewing's sarcoma patient’s plasma samples and biopsies. Initially, the ES group was compared with the control counterpart. In a next step, the ES arm was further stratified into either initially metastatic and non-metastatic, or poor and good chemotherapy responder groups to identify protein expression profiles that can predict metastatic proneness and chemotherapy response, respectively.

2023-12-19 | PXD035812 | Pride

Gain and/or amplification of chromosome 1q are frequently found in Multiple Myeloma (MM).

Project description:Background: Gain and/or amplification of chromosome 1q are frequently found in Multiple Myeloma (MM). The number of 1q copies correlates with a poor prognosis. The aim of this work is to study the impact on the clinical outcome and the trascriptomic changes induced by Gain1q (3 copies of 1q, 3X) and amplification 1q (Amp1q, ≥4 copies of 1q, 4X) in MM patients enrolled in the CoMMpass study (NCT145429). Methods: Fluorescence in situ hybridization (FISH) in CD138+ purified bone marrow plasma cells was centralized and performed at baseline. The cut-off level for Gain1q was 10% of nuclei with ≥3 copies of 1q (3X), while Amp1q was defined as ≥ 20% of nuclei with ≥4 copies of 1q (4X). Transcriptome data from patients were used to find differentially expressed genes (DEGs) in gain (3X) and amp1q (4X) patients.

2023-01-16 | GSE193427 | GEO

Transcriptional profiling of Ewing's sarcoma derived exosomes

Project description:Exosomes are small RNA and protein containing vesicles that can mediate hetero- and homotypic intercellular communication between normal and malignant cells. Especially, tumor-derived exosomes are believed to mediate reprogramming of the tumor-associated stroma to favor tumor growth and metastasis. In this study we isolated exosomes from three different Ewing’s sarcoma (ES) cell lines by ultracentrifugation. Microarray analysis of ES-derived exosomes and their parental cells was performed to gain insight into the spectrum of transcripts they contain and the functions in which these transcripts might be involved in. In total we analyzed six different samples consisting of three pairs of exosomal and cellular RNA of different Ewing's sarcoma cell lines.

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Re-activation of EWS-FLI1 suppressed FOXO1 expression as a novel therapeutic strategy for Ewing´s sarcoma

Project description:Transient transfection of a Ewing's Sarcoma cell line expressing type I EWS-FLI1 fusion and doxycycline-inducible short hairpin RNA against EWS-FLI1 (A673sh)

2013-07-01 | GSE37409 | GEO

Cooperative treatment effectiveness of VE821 and AUY922 in Ewing’s sarcoma cells

Project description:Ewing's sarcoma (ES) is the second most frequent bone cancer during childhood and adolescence originating from a translocation between the EWSR1 and the FLI1 gene, which inactivates BRCA-mediated DNA damage response. Both ATR and HSP90 inhibitors are promising new candidates in the field of ES treatment. We show that the HSP90 inhibitor AUY922 alone induced DNA damages, apoptosis and ER stress, while reducing the abundance of DNA repair proteins. The combinations of the ATR inhibitor VE821 and AUY922 (AUY-VE) led to strong apoptosis induction in ES cell lines, originating from a common set of molecular targets and independent of their p53 status, yet based on different molecular mechanisms. P53 wild-type ES cells activated pro-apoptotic gene transcription and underwent mitochondria-mediated apoptosis. P53 null ES cells, however, accumulated higher level of DNA damage, ER stress and autophagy, finally leading to apoptosis. Moreover, AUY-VE treatment compromised ES cell vitality due to impaired PI3K/AKT/mTOR signaling. Unexpectedly, the combinations of AUY922 with the ATM inhibitor, KU55933 failed to kill ES cells and showed protective effects compared to AUY-VE. In summary, we provide mechanistic insights into the effective ES cell killing by ATR and HSP90 inhibitor combinations, which also offers a targetable approach for BRCA-deficient tumors, irrespective of their p53 status and may give rise to new therapeutic strategies.

2021-09-09 | PXD021562 | Pride

Single cell RNA-seq of seizure-affected brain tissue with mosaic copy number gain of chromosome 1q

Project description:Somatic mosaicism is a known cause of neurological disorders, including developmental brain malformations and epilepsy. Brain mosaic copy number gain of chromosome 1q is associated with cortical malformations, early-onset epilepsy, and developmental delay. Pathogenic brain mosaicism is traditionally attributed to post-zygotic genetic alterations arising in a neural progenitor cell during fetal development. However, in our cohort, in at least five of six patients with brain mosaic copy number gain of chromosome 1q, the alteration occurred pre-conception. We observed a third non-constitutive, but parentally-derived, haplotype for chromosome 1q in patient brain tissue, demonstrating that the copy number alteration occurred in a gamete pre-conception. The altered cells had no representation in parental buccal or proband blood or buccal samples, but were prominently observed in proband brain tissue, suggesting the copy number gain was lost in most cell lineages during embryonic development. Single-nuclei genotyping coupled with gene expression profiling revealed a strong enrichment of the chromosome 1q gain in astrocytes, which correlated with the unusual finding of hyaline astrocytic inclusions in all six cases.

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