Factors Affecting EWS-FLI1 Activity in Ewing's Sarcoma

Herrero-Martín, David; Fourtouna, Argyro; Niedan, Stephan; Riedmann, Lucia T.; Schwentner, Raphaela; Aryee, Dave N.T.

doi:10.1155/2011/352580

Cited by 19 publications

(28 citation statements)

References 134 publications

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“…EWS-FLI1 does not transform human cells in vitro , suggesting that the cooperating mutations or related parallel pathways are essential for pathogenesis [18]. Related pathways include p53, INK4A, IGF-1/IGF-1R, bFGF, CD99, and a list of other tyrosine kinase and Wnt pathways [1, 37]. MicroRNAs (miRNAs) are well described in adult cancers and either block target miRNA expression or cause degradation.…”

Section: Fusion Proteins and Targetsmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are well described in adult cancers and either block target miRNA expression or cause degradation. miRNA-145 has been described as the most active in ESFTs, but other works have shown that other miRNAs could have comparable modulatory effects [37]. Further study of the above pathways, along with RNA processing factors, may shed light onto the specific molecular therapies that could be effective in treating ES/ESFTs.…”

Section: Fusion Proteins and Targetsmentioning

confidence: 99%

“…Other potential strategies include the use of small interfering RNAs (siRNA), YK-4-279 to block RNA helicase A binding, O-linked beta-N-acetylglucosamine, miRNA (specifically miRNA-145) targeting, and various antiangiogenic and antivascular strategies [15, 37, 70]. …”

Section: Clinical Approaches and Targeted Therapeuticsmentioning

confidence: 99%

“…However, due to the fact that these types of therapeutics are challenging to administer pharmacologically, they are not necessarily applicable clinically, and several groups have asserted that the next reasonable step is focusing on protein-protein interactions rather than the ESFT genes themselves [15, 37, 74]. In contrast, insulin-like growth factor receptor-1 (IGF-1R) antagonists include a list of antibodies and tyrosine kinase inhibitors, which have shown responses in phase I and phase II clinical trials.…”

Section: Clinical Approaches and Targeted Therapeuticsmentioning

confidence: 99%

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The Biology of Ewing Sarcoma

et al. 2013

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Objective. The goal of this study was to review the current literature on the biology of Ewing's sarcoma, including current treatments and the means by which an understanding of biological mechanisms could impact future treatments. Methods. A search of PubMed and The Cochrane Collaboration was performed. Both preclinical and clinical evidence was considered, but specific case reports were not. Primary research articles and reviews were analyzed with an emphasis on recent publications. Results. Ewing sarcoma is associated with specific chromosomal translocations and the resulting transcripts/proteins. Knowledge of the biology of Ewing sarcoma has been growing but has yet to significantly impact or produce new treatments. Localized cases have seen improvements in survival rates, but the same cannot be said of metastatic and recurrent cases. Standard surgical, radiation, and chemotherapy treatments are reaching their efficacy limits. Conclusion. Improving prognosis likely lies in advancing biomarkers and early diagnosis, determining a cell(s) of origin, and developing effective molecular therapeutics and antiangiogenic agents. Preclinical evidence suggests the utility of molecular therapies for Ewing sarcoma. Early clinical results also reveal potential for novel treatments but require further development and evaluation before widespread use can be advocated.

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Section: Fusion Proteins and Targetsmentioning

confidence: 99%

Section: Fusion Proteins and Targetsmentioning

confidence: 99%

Section: Clinical Approaches and Targeted Therapeuticsmentioning

confidence: 99%

Section: Clinical Approaches and Targeted Therapeuticsmentioning

confidence: 99%

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The Biology of Ewing Sarcoma

et al. 2013

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“…The functional consequences of heterodimerization between EWS/FLI1 and EWS on RNA splicing also have to be revealed [19,50].…”

Section: The Common Role Of Ews and Ews/fli In Transcription And Splimentioning

confidence: 99%

Functional Interactions in Transcription and Splicing of Ewing’s Sarcoma

Todorova

2013

ISRN Genetics

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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.

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Disruption of mammalian SWI/SNF and polycomb complexes in human sarcomas: mechanisms and therapeutic opportunities

McBride

Kadoch

2018

The Journal of Pathology

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Factors Affecting EWS-FLI1 Activity in Ewing's Sarcoma

Cited by 19 publications

References 134 publications

The Biology of Ewing Sarcoma

The Biology of Ewing Sarcoma

Functional Interactions in Transcription and Splicing of Ewing’s Sarcoma

Disruption of mammalian SWI/SNF and polycomb complexes in human sarcomas: mechanisms and therapeutic opportunities

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