ArticleSarcoma2011
Targeted Therapy of Ewing's Sarcoma.
Article in Sarcoma, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Antitumor Activity of Lurbinectedin, a Selective Inhibitor of Oncogene Transcription, in Patients with Relapsed Ewing Sarcoma: Results of a Basket Phase II Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Phase Ib/II Study of the Safety and Efficacy of Combination Therapy with Multikinase VEGF Inhibitor Pazopanib and MEK Inhibitor Trametinib In Advanced Soft Tissue Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- ASO Author Reflections: Current Status and Future Directions of Ewing Sarcoma Research.Annals of surgical oncology · 2025Article
- Primitive neuroectodermal tumor of the kidney: A rare case with unusual presentation.Medical journal, Armed Forces India · 2020Article
- Clinical genomic profiling to identify actionable alterations for investigational therapies in patients with diverse sarcomas.Oncotarget · 2017Article
- PRAS40 deregulates apoptosis in Ewing sarcoma family tumors by enhancing the insulin receptor/Akt and mTOR signaling pathways.American journal of cancer research · 2016Article
- 3D tissue-engineered model of Ewing's sarcoma.Advanced drug delivery reviews · 2014Review
- Prospects and pitfalls of personalizing therapies for sarcomas: from children, adolescents, and young adults to the elderly.Current oncology reports · 2014Review
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- Potential molecular targets for Ewing's sarcoma therapy.Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology · 2012Article
- Ewing's sarcoma: overcoming the therapeutic plateau.Discovery medicine · 2012Article
- Targeted therapy in bone and soft tissue sarcoma in children and adolescents.Current oncology reports · 2012Review
- Molecular pathogenesis and targeted therapeutics in Ewing sarcoma/primitive neuroectodermal tumours.Clinical sarcoma research · 2012Article
- MAPK/ERK Signaling in Osteosarcomas, Ewing Sarcomas and Chondrosarcomas: Therapeutic Implications and Future Directions.Sarcoma · 2012Article
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- Factors Affecting EWS-FLI1 Activity in Ewing's Sarcoma.Sarcoma · 2011Article
- EWING'S SARCOMA: EPIDEMIOLOGY AND PROGNOSIS FOR PATIENTS TREATED AT THE PEDIATRIC ONCOLOGY INSTITUTE, IOP-GRAACC-UNIFESP.Revista brasileira de ortopediaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Refractory and/or recurrent Ewing's sarcoma (EWS) remains a clinical challenge because the disease's resistance to therapy makes it difficult to achieve durable results with standard treatments that include chemotherapy, radiation, and surgery. Recently, insulin-like-growth-factor-1-receptor (IGF1R) antibodies have been shown to have a modest single-agent activity in EWS. Patient selection using biomarkers and understanding response and resistance mechanisms in relation to IGF1R and mammalian target of rapamycin pathways are areas of active research. Since EWS has a unique tumor-specific EWS-FLI1 t(11;22) translocation and oncogenic fusion protein, inhibition of EWS-FLI1 transcription, translation, and/or protein function may be key to eradicating EWS at the stem-cell level. Recently, a small molecule that blocks the protein-protein interaction of EWS-FLI1 with RNA helicase A has been shown in preclinical models to inhibit EWS growth. The successful application of this first-in-class protein-protein inhibitor in the clinic could become a model system for translocation-associated cancers such as EWS.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.