Microarray analysis of Ewing’s sarcoma family of tumours reveals characteristic gene expression signatures associated with metastasis and resistance to chemotherapy

2008 ◽  
Vol 44 (5) ◽  
pp. 699-709 ◽  
Author(s):  
Karl-Ludwig Schaefer ◽  
Martin Eisenacher ◽  
Yvonne Braun ◽  
Kristin Brachwitz ◽  
Daniel H. Wai ◽  
...  
2004 ◽  
Vol 110 (5) ◽  
pp. 687-694 ◽  
Author(s):  
Claudia Baer ◽  
Mattias Nees ◽  
Stephen Breit ◽  
Barbara Selle ◽  
Andreas E. Kulozik ◽  
...  

2009 ◽  
Vol 183 (3) ◽  
pp. 1975-1982 ◽  
Author(s):  
Qingsheng Li ◽  
Anthony J. Smith ◽  
Timothy W. Schacker ◽  
John V. Carlis ◽  
Lijie Duan ◽  
...  

2020 ◽  
Author(s):  
Jie Jiang ◽  
Chong Liu ◽  
Guoyong Xu ◽  
Tuo Liang ◽  
Chaojie Yu ◽  
...  

Abstract Background: Ewing's sarcoma (ES) is the second most prevalent malignancy among bone tissue tumors, and there is no adequate prognosis biomarker. The protein encoded by CCT6A is a molecular chaperone. Early studies have suggested that CCT6A is involved in the development of many cancers, however, there is no clear evidence of a role for CCT6A in ES.Methods: In this study, we performed a bioinformatics analysis of 32 Ewing sarcoma specimens from the GSE17618 dataset for differences in gene expression and overall survival, event-free survival, and gene expression in different subgroups. Results: After three screenings, we identified CCT6A as highly correlated with Ewing's sarcoma prognosis. Survival analysis showed low overall survival (OS) for CCT6A high expression (P=0.024). On the other hand, Cox regression analysis showed that CCT6A expression, event-free survival (EFS), and age were strongly associated with the prognosis of Ewing sarcoma, identified as independent poor prognostic biomarkers. (CCT6A: P=0.015; Age: P-value=0.026; EFS: P-value=0.001). Conclusion: The expression level of CCT6A is strongly associated with the prognosis of Ewing's sarcoma. High expression of the CCT6A gene may serve as a biomarker for poor prognosis in patients with Ewing's sarcoma.


ISRN Genetics ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Roumiana Todorova

Ewing’s sarcoma (EWS) protein is a member of the TET (TLS/EWS/TAF15) family of RNA and DNA-binding proteins with unknown cellular role. EWS protein is encoded by the EWS oncogene on chromosome 22q12, a target of chromosomal translocations in Ewing’s sarcoma tumors. The exact mechanism of EWS participation in gene expression and pathogenesis of the resulting cancers is not defined. The binding partners of native EWS and EWS fusion proteins (EFPs) are described schematically in a model, an attempt to link the transcription with the splicing. The experimental data about the partnerships of EWS and EFPs are summarized, which may lead to better understanding of their function.


2010 ◽  
Author(s):  
Idriss M. Bennani-Baiti ◽  
Elizabeth R. Lawlor ◽  
Aaron Cooper ◽  
Maximilian Kauer ◽  
Jozef Ban ◽  
...  

2012 ◽  
Vol 131 (9) ◽  
pp. 2153-2164 ◽  
Author(s):  
Aleksandar Boro ◽  
Kathya Prêtre ◽  
Florian Rechfeld ◽  
Verena Thalhammer ◽  
Susanne Oesch ◽  
...  

2015 ◽  
Vol 117 (8) ◽  
pp. 824-828 ◽  
Author(s):  
Paolo Fagone ◽  
Ferdinando Nicoletti ◽  
Lucia Salvatorelli ◽  
Giuseppe Musumeci ◽  
Gaetano Magro

2020 ◽  
Author(s):  
Shijie Gao ◽  
Guowang Li ◽  
Hao Yu ◽  
Shiyang Yuan ◽  
Wenxiang Li ◽  
...  

Abstract Background DNA methylation is a common epigenetic regulatory way, and it plays a critical role in various human diseases. However, the potential role of how DNA methylation impacts Ewing’s sarcoma (ES) is not clear. This study aimed to explore the regulatory role of DNA methylation in ES. Methods The microarray data of gene expression and methylation were downloaded from Gene Expression Omnibus (GEO) database, and analyzed via GEO2R. Venn analysis was then applied to identify aberrantly methylated differentially expressed genes (DEGs). Subsequently, Function and pathway enrichment analysis was conducted. Protein-protein interaction (PPI) network was constructed. Hub genes were determined. Besides, a connectivity map (CMap) analysis was performed to screen bioactive compounds for ES treatment. Results A total of 135 hypomethylated high expression genes and 523 hypermethylated low expression genes were identified. The hypomethylated high expression genes were enriched in signal transduction and the apoptosis process. Meanwhile, hypermethylated low expression genes were related to DNA replication and transcription regulation. We next determined 10 hub genes through PPI analysis, among them, C3, TF, and TCEB1 might serve as diagnostic and therapeutic targets. Furthermore, CMap analysis revealed 6 chemicals as potential options for ES treatment. Conclusions For the first time, we jointly analyzed gene profiling and methylation data about ES. The introduction of DNA methylation characteristics over DEGs is helpful to understand the pathogenesis of ES. The identified hub aberrantly methylated DEGs and chemicals might provide some novel insights on ES treatment.


2021 ◽  
Author(s):  
Shijie Gao ◽  
Guowang Li ◽  
Hao Yu ◽  
Shiyang Yuan ◽  
Wenxiang Li ◽  
...  

Abstract Background: DNA methylation is a common epigenetic regulatory way, and it plays a critical role in various human diseases. However, the potential role of how DNA methylation impacts Ewing’s sarcoma (ES) is not clear. This study aimed to explore the regulatory role of DNA methylation in ES.Methods: The microarray data of gene expression and methylation were downloaded from Gene Expression Omnibus (GEO) database, and analyzed via GEO2R. Venn analysis was then applied to identify aberrantly methylated differentially expressed genes (DEGs). Subsequently, Function and pathway enrichment analysis was conducted. Protein-protein interaction (PPI) network was constructed. Hub genes were determined. Besides, a connectivity map (CMap) analysis was performed to screen bioactive compounds for ES treatment.Results: A total of 135 hypomethylated high expression genes and 523 hypermethylated low expression genes were identified. The hypomethylated high expression genes were enriched in signal transduction and the apoptosis process. Meanwhile, hypermethylated low expression genes were related to DNA replication and transcription regulation. We next determined 10 hub genes through PPI analysis, among them, C3, TF, and TCEB1 might serve as diagnostic and therapeutic targets. Furthermore, CMap analysis revealed 6 chemicals as potential options for ES treatment. Conclusions: For the first time, we jointly analyzed gene profiling and methylation data about ES. The introduction of DNA methylation characteristics over DEGs is helpful to understand the pathogenesis of ES. The identified hub aberrantly methylated DEGs and chemicals might provide some novel insights on ES treatment.


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