Gene expression profiling and array CGH in Ewing's sarcoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE8303 | GEO | 2007/11/15
SECONDARY ACCESSION(S): PRJNA101269
REPOSITORIES: GEO
Similar Datasets
Project description:Ewing’s Sarcoma (ES) is characterized by specific chromosomal translocations, the most common being t(11;22)(q24;q12). Additionally, other types of genetic abnormalities may occur and be relevant to explain the variable tumoural biology and clinical outcome. We have carried out a high-resolution array CGH and expression profiling on 25 ES tumour samples to characterize the DNA copy number aberrations (CNA) occurring in these tumours and to determine their association with gene expression profiles (GEO Series accession number: GSE8303) and their clinical outcome. CNA were observed in 84% of the cases. We observed a median number of 3 aberrations per case. Besides numerical chromosomal changes, smaller aberrations were found and defined at chromosomes 5p, 7q and 9p. All CNA were compiled to define the smallest overlapping regions of imbalance (SORI). Thirty five SORI were delimited. Bioinformatic analyses were conducted to identify subgroups according to the pattern of genomic instability obtained. Unsupervised and supervised clustering analyses (using SORI as variables) segregated the tumours into two distinct groups: one genomically stable (≤ 3 CNA) and another genomically unstable one (> 3 CNA). The genomic unstable group showed a statistically significant shorter overall survival and was more refractory to chemotherapy. This report elucidates data about genomic instability in ES, based on CNA and expression profiling for the first time, and shows that a genomically unstable group of Ewing tumours is correlated with a significant poor prognosis. Keywords: Comparative Genomic Hybridization - array; Genomic Instability
2007-11-09 | GSE8398 | GEO
Project description:Ewingâs Sarcoma (ES) is characterized by specific chromosomal translocations, the most common being t(11;22)(q24;q12). Additionally, other types of genetic abnormalities may occur and be relevant to explain the variable tumoural biology and clinical outcome. We have carried out a high-resolution array CGH and expression profiling on 25 ES tumour samples to characterize the DNA copy number aberrations (CNA) occurring in these tumours and to determine their association with gene expression profiles (GEO Series accession number: GSE8303) and their clinical outcome. CNA were observed in 84% of the cases. We observed a median number of 3 aberrations per case. Besides numerical chromosomal changes, smaller aberrations were found and defined at chromosomes 5p, 7q and 9p. All CNA were compiled to define the smallest overlapping regions of imbalance (SORI). Thirty five SORI were delimited. Bioinformatic analyses were conducted to identify subgroups according to the pattern of genomic instability obtained. Unsupervised and supervised clustering analyses (using SORI as variables) segregated the tumours into two distinct groups: one genomically stable (⤠3 CNA) and another genomically unstable one (> 3 CNA). The genomic unstable group showed a statistically significant shorter overall survival and was more refractory to chemotherapy. This report elucidates data about genomic instability in ES, based on CNA and expression profiling for the first time, and shows that a genomically unstable group of Ewing tumours is correlated with a significant poor prognosis. Experiment Overall Design: Comparative experiment: pheripheral blood pool of ten healthy female donors: CONTROL vs. 26 Ewing Sarcoma Tumour Samples. Experiment Overall Design: Note that although 26 samples were profiled, only 25 were analysed (sample #11 did not pass quality control).
2008-06-16 | E-GEOD-8398 | biostudies-arrayexpress
Project description:Background: Osteosarcoma (OS) tumors and derived cell lines are characterized by complex chromosomal abnormalities. The availability of molecular genome profiling techniques such as array CGH have markedly enabled the high-resolution genome analysis of tumor genomes, as well as helped elucidate the mechanisms leading to their complexity. The identification of tumor-specific genomic profiles is currently the focus of many array CGH studies, but there have been no analyses to date documenting the genomic signatures consistent with chromosomal instability mechanisms in OS. Results: In this study we utilized high-resolution oligonucleotide array CGH to interrogate recurrent signatures of genomic imbalance in 10 OS tumors that were consistent with the breakage fusion bridge(BFB) mechanism. Comparative analysis of the tumors showed that they exhibited varying levels of genomic imbalance. The analysis also highlighted three chromosomal regions (6p21 ~ p22, 8q24 and 17p11.2 ~ p12) that were consistently involved in high level gain or amplification events. These three regions have been previously shown by us to be not only involved in high-level imbalance in OS-derived cell lines, but also to exhibit similar imbalance profiles consistent with BFB-related events. Karyotype and dual-color FISH analysis showed that repeated rearrangements of these unstable chromosomes through BFB cycles may create a heterogeneous pattern of copy number alterations. Conclusions: This genome-wide analysis is the first to utilize oligonucleotide array CGH and FISH analysis to derive possible genomic signatures of chromosomal instability in OS tumors. Perpetuation of the BFB cycle will create a heterogeneous pattern of copy number alterations by repeated rearrangement of the unstable tumor genome., thereby generating diverse phenotypes The resulting phenotypic diversity can generate tumors with a propensity for an aggressive disease course. A better understanding of the underlying mechanisms events leading to tumor development could result in the identification of prognostic markers and therapeutic targets. Keywords: osteosarcoma, chromosomal instability, gene amplification, breakage-fusion-bridge cycle, oligonucleotide array comparative genomic hybridization
2007-11-21 | GSE9654 | GEO
Project description:Genomic characterization of mesothelioma patients by CGH arrays. Genomic characterization of mesothelioma patients by CGH arrays.
2018-04-01 | GSE67487 | GEO
Project description:Dysfunction in type I interferon (IFN) signaling occurs in patients with stage II or more advanced cancer. After screening the effects of a panel of 12 melanoma cell lines on PBMCs of healthy volunteers of IFNalpha signal pathway, two groups of melanoma cell lines could be identified one with stronger suppression (low pSTAT-1 group) than the other (high pSTAT-1 group). Comparative genomic hybridization (CGH) identified consistent amplification of 12q22-24 as a genomic marker for the immune suppressive melanoma cell lines. This region corresponded to higher transcription of the NOS1 gene located in that region in the low pSTAT1 group and NOS1 expression was identified as causal factor in melanoma induced immune suppression.
2015-03-01 | GSE44850 | GEO
Project description:Ewing sarcoma a rare pediatric tumor characterized by EWSR1-ETS fusions. We performed expression profiling of both miRNA and mRNA from the same Ewing's sarcoma tumors. We propose a novel statistical measure of non-linear dependence between miRNA and mRNA expression, In order to infer miRNA-target interactions. This approach, That we name antagonism pattern detection, Is based on the statistical recognition of a triangular-shaped pattern in miRNA-target expression profiles. This pattern is observed in miRNA-target expression measurements since their simultaneously elevated expression is statistically under-represented in the case of miRNA silencing effect. The proposed method enables miRNA target prediction to strongly rely on cellular context and physiological conditions reflected by expression data. Expression profiling of Ewing sarcoma samples in the frame of the CIT program from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net).
2012-06-12 | GSE37371 | GEO
Project description:Ewing sarcoma a rare pediatric tumor characterized by EWSR1-ETS fusions. We performed expression profiling of both miRNA and mRNA from the same Ewing's sarcoma tumors. We propose a novel statistical measure of non-linear dependence between miRNA and mRNA expression, In order to infer miRNA-target interactions. This approach, That we name antagonism pattern detection, Is based on the statistical recognition of a triangular-shaped pattern in miRNA-target expression profiles. This pattern is observed in miRNA-target expression measurements since their simultaneously elevated expression is statistically under-represented in the case of miRNA silencing effect. The proposed method enables miRNA target prediction to strongly rely on cellular context and physiological conditions reflected by expression data.
2012-06-12 | GSE37370 | GEO
Project description: Not available
| S-EPMC6984994 | biostudies-literature
Project description: Not available
| S-EPMC2968715 | biostudies-literature