ArticleOncogene1999
Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 108 citations in OpenAlex.
- Tumoral TP53 and/or CDKN2A alterations are not reliable prognostic biomarkers in patients with localized Ewing sarcoma: a report from the Children's Oncology Group.Pediatric blood & cancer · 2015Trial
- Evaluation of polymorphisms in EWSR1 and risk of Ewing sarcoma: a report from the Childhood Cancer Survivor Study.Pediatric blood & cancer · 2012Trial
- Bioinformatic Analysis of Recurrent Genomic Alterations and Corresponding Pathway Alterations in Ewing Sarcoma.Journal of personalized medicine · 2023Article
- Extracellular vesicle-associated IGF2BP3 tunes Ewing sarcoma cell migration and affects PI3K/Akt pathway in neighboring cells.Cancer gene therapy · 2023Article
- Comparative structure analysis of the ETSi domain of ERG3 and its complex with the E74 promoter DNA sequence.Acta crystallographica. Section F, Structural biology communications · 2018Article
- EWS-FLI1 positively regulates autophagy by increasing ATG4B expression in Ewing sarcoma cells.International journal of molecular medicine · 2017Article
- EWSR1/ELF5 induces acute myeloid leukemia by inhibiting p53/p21 pathway.Cancer science · 2016Article
- EWSR1 regulates mitosis by dynamically influencing microtubule acetylation.Cell cycle (Georgetown, Tex.) · 2016Article
- BET bromodomain inhibitors suppress EWS-FLI1-dependent transcription and the IGF1 autocrine mechanism in Ewing sarcoma.Oncotarget · 2016Article
- Cancer stem cells in pediatric sarcomas.Frontiers in oncology · 2013Article
- Ewing sarcoma/peripheral primitive neuroectodermal tumor and related tumors.Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society · 2012Review
- Promiscuous partnerships in Ewing's sarcoma.Cancer genetics · 2011Review
- Oncogenic fusion protein EWS/FLI1 down-regulates gene expression by both transcriptional and posttranscriptional mechanisms.The Journal of biological chemistry · 2011Article
- Nonredundant functions for Akt isoforms in astrocyte growth and gliomagenesis in an orthotopic transplantation model.Cancer research · 2011Article
- Article
- Pathology of Ewing's sarcoma/PNET: Current opinion and emerging concepts.Indian journal of orthopaedics · 2010Article
- Review
- Soft tissue tumors associated with EWSR1 translocation.Virchows Archiv : an international journal of pathology · 2010Review
- Stable interference of EWS-FLI1 in an Ewing sarcoma cell line impairs IGF-1/IGF-1R signalling and reveals TOPK as a new target.British journal of cancer · 2009Article
- IGF1 is a common target gene of Ewing's sarcoma fusion proteins in mesenchymal progenitor cells.PloS one · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ewing's sarcomas express chimeric transcription factors resulting from a fusion of the amino terminus of the EWS gene to the carboxyl terminus of one of five ETS proteins. While the majority of tumors express EWS/FLI1 fusions, some Ewing's tumors contain variant chimeras such as EWS/ETV1 that have divergent ETS DNA-binding domains. In spite of their structural differences, both EWS/ETS fusions up regulate EAT-2, a previously described EWS/FLI1 target gene. In contrast to EWS/FLI1, NIH3T3 cells expressing EWS/ETV1 cannot form colonies in soft agar though coexpression of a dominant negative truncated ETV1 construct attenuates EWS/FLI1 mediated anchorage independent growth. When EWS/ETV1 or EWS/FLI1 expressing NIH3T3 cells are injected into SCID mice, tumors form more often and faster than with NIH-3T3 cells with empty vector controls. The tumorigenic potency of each EWS/ETS fusion is linked to its C-terminal structure, with the FLI1 C-terminus confering a greater tumorigenic potential than the corresponding ETV1 domain. The resulting EWS/ETV1 and EWS/FLI1 tumors closely resemble each other at both a macroscopic and a microscopic level. These tumors differ greatly from tumors formed by NIH3T3 cells expressing activated RAS. These data indicate that in spite of their structural differences, EWS/ETV1 and EWS/FLI1 promote oncogenesis via similar biologic pathways.
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