ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
Identification of genes regulated by the EWS/NR4A3 fusion protein in extraskeletal myxoid chondrosarcoma.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- From pathogenesis to the patient's bedside: a comprehensive review of extraskeletal myxoid chondrosarcoma.Journal of cancer research and clinical oncology · 2025Review
- The role of radiotherapy and chemotherapy in extraskeletal myxoid chondrosarcoma.Journal of orthopaedic surgery and research · 2025Article
- Extraskeletal Myxoid Chondrosarcoma: State of the Art and Current Research on Biology and Clinical Management.Cancers · 2020Review
- Extraskeletal Myxoid Chondrosarcomas: Combined Modality Therapy With Both Radiation and Surgery Improves Local Control.American journal of clinical oncology · 2019Article
- INSM1 expression and its diagnostic significance in extraskeletal myxoid chondrosarcoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- EWSR1 regulates mitosis by dynamically influencing microtubule acetylation.Cell cycle (Georgetown, Tex.) · 2016Article
- The interplay of NR4A receptors and the oncogene-tumor suppressor networks in cancer.Cellular signalling · 2015Review
- The orphan nuclear receptors at their 25-year reunion.Journal of molecular endocrinology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 75 % of extraskeletal myxoid chondrosarcoma tumors (EMC) harbor a t(9;22) chromosome translocation generating an EWS/NR4A3 fusion protein that is thought to be instrumental in the tumoral process. Current evidence suggests that one function of the fusion protein is to overexpress target genes. We have generated an in vitro human cellular model in which the fusion protein is expressed in mesenchymal bone marrow stem cells. We have performed microarray analyses of these cells and identified several genes overexpressed in the presence of EWS/NR4A3 which are also overexpressed in EMC tumors. These genes and their products represent potential therapeutic targets for EMC tumors.
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