Machiela et al. (2018). Genome-wide association study identifies multiple new loci associated with Ewing sarcoma susceptibility. Nature Communications.
Baldauf et al. (2018). Are EWSR1-NFATc2-positive sarcomas really Ewing sarcomas?. Modern Pathology.
Tsafou et al. (2018). Targeting Intrinsically Disordered Transcription Factors: Changing the Paradigm. Journal of Molecular Biology.
Gorthi et al. (2018). EWS–FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma. Nature.
Çelik et al. (2018). Clofarabine inhibits Ewing sarcoma growth through a novel molecular mechanism involving direct binding to CD99. Oncogene.
Baldauf et al. (2017). Robust diagnosis of Ewing sarcoma by immunohistochemical detection of super-enhancer-driven EWSR1-ETS targets. Oncotarget.
Hamilton et al. (2017). Long-term Outcomes and Complications in Pediatric Ewing Sarcoma. American Journal of Clinical Oncology.
Johnson et al. (2017). Role for the EWS domain of EWS/FLI in binding GGAA-microsatellites required for Ewing sarcoma anchorage independent growth. Proceedings of the National Academy of Sciences.
Sizemore et al. (2017). The ETS family of oncogenic transcription factors in solid tumours. Nature Reviews Cancer.
Sechler et al. (2017). The histone demethylase KDM3A and its downstream target MCAM, promote Ewing Sarcoma cell migration and metastasis. Oncogene.
Marina et al. (2017). Longitudinal follow-up of adult survivors of Ewing sarcoma: A report from the Childhood Cancer Survivor Study. Cancer.
Mutz et al. (2017). EWS-FLI1 confers exquisite sensitivity to NAMPT inhibition in Ewing sarcoma cells. Oncotarget.
Brohl et al. (2017). Frequent inactivating germline mutations in DNA repair genes in patients with Ewing sarcoma. Genetics in Medicine.
Gardiner et al. (2017). C/EBP\upbeta{}{-}{1} promotes transformation and chemoresistance in Ewing sarcoma cells. Oncotarget.
Sheffield et al. (2017). DNA methylation heterogeneity defines a disease spectrum in Ewing sarcoma. Nature Medicine.
Schwentner et al. (2016). The role of miR-17-92 in the miRegulatory landscape of Ewing sarcoma. Oncotarget.
Gordon et al. (2016). Modeling the initiation of Ewing sarcoma tumorigenesis in differentiating human embryonic stem cells. Oncogene.
Goss, and Gordon (2016). Gene expression signature based screening identifies ribonucleotide reductase as a candidate therapeutic target in Ewing sarcoma. Oncotarget.
Krook et al. (2016). A bivalent promoter contributes to stress-induced plasticity of CXCR4 in Ewing sarcoma. Oncotarget.
Cash et al. (2016). Comparison of clinical features and outcomes in patients with extraskeletal versus skeletal localized Ewing sarcoma: A report from the Children\textquotesingles Oncology Group. Pediatric Blood {\&} Cancer.
Hingorani et al. (2016). Current state of pediatric sarcoma biology and opportunities for future discovery: A report from the sarcoma translational research workshop. Cancer Genetics.
Minas et al. (2016). Combined experience of six independent laboratories attempting to create an Ewing sarcoma mouse model. Oncotarget.
Theisen et al. (2016). Therapeutic opportunities in Ewing sarcoma: EWS-FLI inhibition via LSD1 targeting. Oncotarget.
Osgood et al. (2016). Identification of Mithramycin Analogues with Improved Targeting of the EWS-FLI1 Transcription Factor. Clin. Cancer Res.
Kovar et al. (2016). The second European interdisciplinary Ewing sarcoma research summit – A joint effort to deconstructing the multiple layers of a complex disease. Oncotarget.
Zhang et al. (2015). Germline Mutations in Predisposition Genes in Pediatric Cancer. N. Engl. J. Med.
Gaspar et al. (2015). Ewing Sarcoma: Current Management and Future Approaches Through Collaboration. Journal of Clinical Oncology.
Abbott et al. (2015). Abstract 2748: A population-based survey of excess cancers observed in Ewing\textquotesingles sarcoma and in their first-, second-, and third-degree relatives. Cancer Res.
Gomez, and Davis (2015). Linking germline and somatic variation in Ewing sarcoma. Nat. Genet.
Agelopoulos et al. (2015). Deep Sequencing in Conjunction with Expression and Functional Analyses Reveals Activation of FGFR1 in Ewing Sarcoma. Clin. Cancer Res.
Grünewald et al. (2015). Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite. Nat. Genet.
Sand et al. (2015). Sequencing Overview of Ewing Sarcoma: A Journey across Genomic, Epigenomic and Transcriptomic Landscapes. International Journal of Molecular Sciences.
Fadul et al. (2015). EWS/FLI utilizes NKX2-2 to repress mesenchymal features of Ewing sarcoma. Genes \& cancer.
Selvanathan et al. (2015). Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing. Proceedings of the National Academy of Sciences.
Tang et al. (2015). SLFN11 Is a Transcriptional Target of EWS-FLI1 and a Determinant of Drug Response in Ewing Sarcoma. Clin. Cancer Res.
Schwentner et al. (2015). EWS-FLI1 employs an E2F switch to drive target gene expression. Nucleic Acids Res.
Tomazou et al. (2015). Epigenome mapping reveals distinct modes of gene regulation and widespread enhancer reprogramming by the oncogenic fusion protein EWS-FLI1. Cell Reports.
Lawlor, and Sorensen (2015). Twenty Years on: What Do We Really Know about Ewing Sarcoma and What Is the Path Forward?. Crit. Rev. Oncog.
Choy et al. (2014). Phase II study of olaparib in patients with refractory Ewing sarcoma following failure of standard chemotherapy. {BMC} Cancer.
Riggi et al. (2014). EWS-FLI1 Utilizes Divergent Chromatin Remodeling Mechanisms to Directly Activate or Repress Enhancer Elements in Ewing Sarcoma. Cancer Cell.
Cornaz-Buros et al. (2014). Targeting Cancer Stem-like Cells as an Approach to Defeating Cellular Heterogeneity in Ewing Sarcoma. Cancer Res.
Crompton et al. (2014). The Genomic Landscape of Pediatric Ewing Sarcoma. Cancer Discovery.
Tirode et al. (2014). Genomic Landscape of Ewing Sarcoma Defines an Aggressive Subtype with Co-Association of STAG2 and TP53 Mutations. Cancer Discovery.
Toretsky, and Wright (2014). Assemblages: functional units formed by cellular phase separation. The Journal of cell biology.
Monument et al. (2014). Clinical and Biochemical Function of Polymorphic NR0B1 GGAA-Microsatellites in Ewing Sarcoma: A Report from the Children\textquotesingles Oncology Group. {PLoS} {ONE}.
Brohl et al. (2014). The Genomic Landscape of the Ewing Sarcoma Family of Tumors Reveals Recurrent STAG2 Mutation. {PLoS} Genetics.
Shibuya et al. (2014). The combination of CD99 and NKX2.2, a transcriptional target of EWSR1-FLI1, is highly specific for the diagnosis of Ewing sarcoma. Virchows Archiv.
Kayarthodi et al. (2014). Anti-Epileptic Drug Targets Ewing Sarcoma. Journal of Pharmaceutical Sciences and Pharmacology.
Sankar et al. (2014). Reversible LSD1 inhibition interferes with global EWS/ETS transcriptional activity and impedes Ewing sarcoma tumor growth. Clin. Cancer Res.
Sankar et al. (2014). Reversible LSD1 inhibition interferes with global EWS/ETS transcriptional activity and impedes Ewing sarcoma tumor growth. Clin. Cancer Res.
Sankar et al. (2014). Reversible LSD1 Inhibition Interferes with Global EWS/ETS Transcriptional Activity and Impedes Ewing Sarcoma Tumor Growth. Clin. Cancer Res.
Zhou et al. (2014). EWS-FLI-1 regulates the neuronal repressor gene REST, which controls Ewing sarcoma growth and vascular morphology. Cancer.
Walters et al. (2014). JARID2 is a direct target of the PAX3-FOXO1 fusion protein and inhibits myogenic differentiation of rhabdomyosarcoma cells. Oncogene.
Huether et al. (2014). The landscape of somatic mutations in epigenetic regulators across 1,000 paediatric cancer genomes. Nat. Commun.
Gorlick et al. (2013). Children\textquotesingles Oncology Group\textquotesingles 2013 blueprint for research: Bone tumors. Pediatric Blood {\&} Cancer.
Grohar et al. (2013). Dual Targeting of EWS-FLI1 Activity and the Associated DNA Damage Response with Trabectedin and SN38 Synergistically Inhibits Ewing Sarcoma Cell Growth. Clin. Cancer Res.
Stoll et al. (2013). Systems biology of Ewing sarcoma: a network model of EWS-FLI1 effect on proliferation and apoptosis. Nucleic Acids Res.
Niedan et al. (2013). Suppression of FOXO1 is responsible for a growth regulatory repressive transcriptional sub-signature of EWS-FLI1 in Ewing sarcoma. Oncogene.
Bilke et al. (2013). Oncogenic ETS fusions deregulate E2F3 target genes in Ewing sarcoma and prostate cancer. Genome Res.
Sankar et al. (2013). EWS and RE1-Silencing Transcription Factor Inhibit Neuronal Phenotype Development and Oncogenic Transformation in Ewing Sarcoma. Genes \& cancer.
Crompton et al. (2013). High-Throughput Tyrosine Kinase Activity Profiling Identifies FAK as a Candidate Therapeutic Target in Ewing Sarcoma. Cancer Res.
Borinstein (2013). A decade in banking Ewing sarcoma: a report from the Children’s Oncology Group. Frontiers in Oncology.
David et al. (2012). Oncostatin M is a growth factor for Ewing sarcoma. The American journal of pathology.
Sankar et al. (2012). Mechanism and relevance of EWS/FLI-mediated transcriptional repression in Ewing sarcoma. Oncogene.
De Vito et al. (2012). A TARBP2-dependent miRNA expression profile underlies cancer stem cell properties and provides candidate therapeutic reagents in Ewing sarcoma. Cancer Cell.
Lawlor, and Thiele (2012). Epigenetic changes in pediatric solid tumors: promising new targets. Clin. Cancer Res.
Reynolds et al. (2012). NuRD suppresses pluripotency gene expression to promote transcriptional heterogeneity and lineage commitment. Cell stem cell.
Baruchel et al. (2012). A phase 2 trial of trabectedin in children with recurrent rhabdomyosarcoma, Ewing sarcoma and non-rhabdomyosarcoma soft tissue sarcomas: A report from the Children’s Oncology Group. Eur. J. Cancer.
Barber-Rotenberg et al. (2012). Single Enantiomer of YK-4-279 Demonstrates Specificity in Targeting the Oncogene EWS-FLI1. Oncotarget.
Patel et al. (2012). Tumor-specific retargeting of an oncogenic transcription factor chimera results in dysregulation of chromatin and transcription. Genome Res.
Postel-Vinay et al. (2012). Common variants near TARDBP and EGR2 are associated with susceptibility to Ewing sarcoma. Nat. Genet.
Lessnick, and Ladanyi (2012). Molecular pathogenesis of Ewing sarcoma: new therapeutic and transcriptional targets. Annual review of pathology.
Juergens et al. (2011). Preliminary Efficacy of the Anti-Insulin–Like Growth Factor Type 1 Receptor Antibody Figitumumab in Patients With Refractory Ewing Sarcoma. J. Clin. Oncol.
Grohar et al. (2011). Identification of an Inhibitor of the EWS-FLI1 Oncogenic Transcription Factor by High-Throughput Screening. {JNCI} Journal of the National Cancer Institute.
Grohar et al. (2011). Ecteinascidin 743 Interferes with the Activity of EWS-FLI1 in Ewing Sarcoma Cells. Neoplasia.
Desai, and Jambhekar (2010). Pathology of Ewing’s sarcoma/PNET: Current opinion and emerging concepts. Indian journal of orthopaedics.
Erkizan et al. (2010). Oncogenic partnerships: EWS-FLI1 protein interactions initiate key pathways of Ewing’s sarcoma. Clinical cancer research : an official journal of the American Association for Cancer Research.
Ginsberg et al. (2010). Long-term Survivors of Childhood Ewing Sarcoma: Report From the Childhood Cancer Survivor Study. {JNCI} Journal of the National Cancer Institute.
Riggi et al. (2010). EWS-FLI-1 modulates miRNA145 and SOX2 expression to initiate mesenchymal stem cell reprogramming toward Ewing sarcoma cancer stem cells. Genes Dev.
Le Deley et al. (2010). Impact of EWS-ETS fusion type on disease progression in Ewing’s sarcoma/peripheral primitive neuroectodermal tumor: prospective results from the cooperative Euro-E.W.I.N.G. 99 trial. Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
Randall et al. (2010). Is There a Predisposition Gene for Ewing\textquotesingles Sarcoma?. Journal of Oncology.
Erkizan et al. (2009). A small molecule blocking oncogenic protein EWS-FLI1 interaction with RNA helicase A inhibits growth of Ewing\textquotesingles sarcoma. Nature Medicine.
DuBois et al. (2009). Phase II study of intermediate-dose cytarabine in patients with relapsed or refractory Ewing sarcoma: A report from the Children\textquotesingles Oncology Group. Pediatric Blood {\&} Cancer.
Houghton (2009). How do we identify novel treatment for childhood cancer?. Pediatric Blood {\&} Cancer.
Suva et al. (2009). Identification of Cancer Stem Cells in Ewing’s Sarcoma. Cancer Res.
Guillon et al. (2009). The oncogenic EWS-FLI1 protein binds in vivo GGAA microsatellite sequences with potential transcriptional activation function. PLoS One.
Gangwal et al. (2008). Microsatellites as EWS/FLI response elements in Ewing’s sarcoma. Proc. Natl. Acad. Sci. U.S.A.
Esiashvili et al. (2008). Changes in Incidence and Survival of Ewing Sarcoma Patients Over the Past 3 Decades. Journal of Pediatric Hematology/Oncology.
Owen et al. (2008). EWS/FLI mediates transcriptional repression via NKX2.2 during oncogenic transformation in Ewing’s sarcoma. PLoS One.
Stegmaier et al. (2007). Signature-Based Small Molecule Screening Identifies Cytosine Arabinoside as an EWS/FLI Modulator in Ewing Sarcoma. {PLoS} Medicine.
Kinsey et al. (2006). NR0B1 is required for the oncogenic phenotype mediated by EWS/FLI in Ewing’s sarcoma. Molecular cancer research : MCR.
Khoury (2005). Ewing sarcoma family of tumors. Adv. Anat. Pathol.
Torchia et al. (2003). Ewing tumor fusion proteins block the differentiation of pluripotent marrow stromal cells. Cancer research.
Lessnick et al. (2002). The Ewing’s sarcoma oncoprotein EWS/FLI induces a p53-dependent growth arrest in primary human fibroblasts. Cancer Cell.
Potter et al. (2000). Identification and characterization of a new human ETS-family transcription factor, TEL2, that is expressed in hematopoietic tissues and can associate with TEL1/ETV6. Blood.
Amann et al. (1999). Relation of neurological marker expression and EWS gene fusion types in MIC2/CD99-positive tumors of the Ewing family. Hum. Pathol.
Sharrocks et al. (1997). The ETS-domain transcription factor family. The international journal of biochemistry \& cell biology.
Toretsky et al. (1997). The Insulin-like Growth Factor-I Receptor Is Required for EWS/FLI-1 Transformation of Fibroblasts. J. Biol. Chem.
Lessnick et al. (1995). Multiple domains mediate transformation by the Ewing’s sarcoma EWS/FLI-1 fusion gene. Oncogene.
May et al. (1993). The Ewing’s sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1. Mol. Cell. Biol.
May et al. (1993). Ewing sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation.. Proc. Natl. Acad. Sci. U.S.A.
Delattre et al. (1992). Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours. Nature.
Rud et al. (1989). Extraosseous Ewing’s sarcoma. A study of 42 cases. Cancer.
Askin et al. (1979). Malignant small cell tumor of the thoracopulmonary region in childhood.A distinctive clinicopathologic entity of uncertain histogenesis. Cancer.
Olisa et al. (1975). Malignant Tumors in American Black and Nigerian Children: A Comparative Study. Journal of the National Cancer Institute.
Fraumeni, and Glass (1970). Rarity of Ewing’s sarcoma among U.S. Negro children. Lancet (London, England).
Ewing (1921). Diffuse endothelioma of bone. Proc New York Path.