Disease relevance of Sarcoma, Ewing's

• A similar program of phenotypic changes is also seen in spontaneous variants of human neuroblastoma and Ewing's sarcoma cells and in ECM-induced Ewing's sarcoma cells [1].
• The autocrine growth-inhibitory effect of bFGF in Ewing's sarcoma cells may explain the low mitotic activity of Ewing's sarcomas [2].
• We studied the expression and role of c-kit and SCF in cell lines of soft tissue sarcoma of neuroectodermic origin, such as Ewing's sarcoma (ES) and peripheral neuro-ectodermal tumors (PNET) [3].
• Activation of the Fli-1 gene by either chromosomal translocation or viral insertion leads to Ewing's sarcoma in humans and erythroleukemia in mice, respectively [4].
• Levels of soluble intercellular adhesion molecule-1 (ICAM-1) were measured in serum samples taken at diagnosis from pediatric patients with Hodgkin's disease (n = 69), acute lymphoblastic leukemia (n = 28), Wilms' tumor (n = 20), osteosarcoma (n = 17), rhabdomyosarcoma (n = 18), or Ewing's sarcoma (n = 15) [5].

High impact information on Sarcoma, Ewing's

• EWS/FLI1, a fusion gene found in Ewing's sarcoma, encodes a transcriptional regulator and promotes cellular transformation by modulating the transcription of specific target genes [6].
• A second Ewing's sarcoma translocation, t(21;22), fuses the EWS gene to another ETS-family transcription factor, ERG [7].
• Growth of human tumor cells (hepatocarcinoma, Ewing's sarcoma) on an extracellular matrix (ECM) produced by bovine corneal endothelial cells is associated with the adoption of a morphological appearance and growth properties that are not expressed when the cells are maintained on plastic [8].
• In a previous study, Ewing's sarcoma cells and colon carcinoma cells failed to attach to plastic and to dishes coated with various collagen types I, III and IV, but adhered rapidly to extracellular matrix (ECM) produced by cultured corneal endothelial cells [9].
• METHODS: The effect of imatinib on c-kit expression and phosphorylation in Ewing's sarcoma cells was examined by immunoblotting [10].

Chemical compound and disease context of Sarcoma, Ewing's

• Influence of doxorubicin dose intensity on response and outcome for patients with osteogenic sarcoma and Ewing's sarcoma [11].
• Taking aim at Ewing's sarcoma: is KIT a target and will imatinib work [12]?
• Targeted inhibition of tyrosine kinase-dependent autocrine loops, therefore, may be a viable therapeutic strategy for Ewing's sarcoma [10].
• Pretreatment serum lactate dehydrogenase predicting metastatic spread in Ewing's sarcoma [13].
• No benefit of ifosfamide in Ewing's sarcoma: a nonrandomized study of the French Society of Pediatric Oncology [14].

Biological context of Sarcoma, Ewing's

• METHODS: Ewing's sarcoma and neuroblastoma cell lines were treated with two synthetic MMPIs (BB-3103 and A-151011) and examined for apoptosis and expression of FasL and Fas [15].
• 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 [16].
• We have previously demonstrated that the breakpoints of this translocation are clustered in a specific intron of the ERG gene on chromosome 21, which has recently been reported to be involved in Ewing's sarcoma [17].
• Differential transactivation by alternative EWS-FLI1 fusion proteins correlates with clinical heterogeneity in Ewing's sarcoma [18].
• The Ewing's sarcoma (EWS) proto-oncogene can give rise to a variety of different tumors because of the generation of transforming EWS fusion proteins upon chromosomal translocation [19].

Anatomical context of Sarcoma, Ewing's

• However, the p160 antigen was expressed in Ewing's sarcoma, leiomyosarcoma, melanoma, 4 of 9 carcinomas, and neonatal fibroblasts in vitro [20].
• PURPOSE: To determine whether consolidation therapy with high-dose melphalan, etoposide, and total-body irradiation (TBI) with autologous stem-cell support would improve the prognosis for patients with newly diagnosed metastatic Ewing's sarcoma (ES) [21].
• Immunomagnetic purging of Ewing's sarcoma from blood and bone marrow: quantitation by real-time polymerase chain reaction [22].
• They also suggest a close relationship between Ewing's sarcoma and peripheral neural tumors, including the chest wall tumor described by Askin, but only a distant relationship to neuroblastoma [23].
• Although recent data have demonstrated that the chimeric EWS-FLI-1 cDNA isolated from cases of Ewing's sarcoma can transform NIH 3T3 cells, little is known about the basis for this transformation [24].

Gene context of Sarcoma, Ewing's

• These findings therefore identify the repression of IGFBP-3 as a key event in the development of Ewing's sarcoma [25].
• The proximate role of EWS-FLI1 in the pathogenesis of Ewing's sarcoma is thought to involve the activation of as yet largely unknown target genes [18].
• Assay of PAX3 and PAX7 mRNA expression in embryonal rhabdomyosarcoma, neuroblastoma, Ewing's sarcoma, and melanoma cell lines revealed tumor-specific expression patterns similar to the corresponding embryonic lineages [26].
• Ewing's sarcoma family tumors are sensitive to tumor necrosis factor-related apoptosis-inducing ligand and express death receptor 4 and death receptor 5 [27].
• Interaction of the EWS NH2 terminus with BARD1 links the Ewing's sarcoma gene to a common tumor suppressor pathway [28].
• The prognostic performance of nucleophosmin was evaluated immunohistochemically on an additional 34 Ewing's sarcoma cases [29].

Analytical, diagnostic and therapeutic context of Sarcoma, Ewing's

• In the design of future clinical trials for osteogenic sarcoma and Ewing's sarcoma, careful attention should be given to optimizing doxorubicin dose intensity in regimens to be tested [11].
• To determine the in vivo efficacy of TRAIL receptor agonists in Ewing's sarcoma family of tumors, mice with orthotopic xenografts were treated with anti-TRAIL-R2 monoclonal antibody or TRAIL/Apo2L in a model that can identify effects on both primary tumors and metastases [30].
• Therefore, Fas ligand is expressed in Ewing's sarcoma but is not functional, suggesting that Ewing's sarcoma is a potential target for immunotherapy [31].
• We and others have previously demonstrated the diagnostic utility of a reverse transcriptase polymerase chain reaction (RT-PCR) assay for the detection of the t(11;22) encoded EWS/FLI-1 chimeric message in Ewing's sarcoma [32].
• ELISA assays showed IL-15 release in a subset of rhabdomyosarcomas and osteosarcomas, but not in Ewing's sarcoma [33].
• In vivo and in vitro expressed N-terminal sequence of EWS (EAD) and hsRPB7 (RNA pol II) interact in vitro forming a stable complex [34].

References