2010
DOI: 10.4161/cbt.9.9.11511
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The molecular pathogenesis of Ewing sarcoma

Abstract: Ewing sarcoma family tumors (ESFT) are a group of aggressive solid bone and soft tissue malignancies of children and young adults characterized by specific chromosomal translocations that give rise to EWS-ETS aberrant transcription factors. Identification of EWS-ETS target genes and their role in tumor signaling networks together with the unravelling of the cell of origin will facilitate the translation into new treatment modalities for these neoplasms.

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Cited by 66 publications
(59 citation statements)
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References 197 publications
(223 reference statements)
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“…Ewing sarcoma (ES) a bone and soft tissue malignancy is characterized by early metastasis to lung and bone [1]. Here we observed genes such as HOXD10, HOXD11 and HOXD13 normally involved in bone formation and ossification pattern of bones [22], to be HOXD locus including HOXD9 and HOXD12 where not uniquely up-regulated in primary ES compared to other tumors.…”
Section: Discussionmentioning
confidence: 68%
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“…Ewing sarcoma (ES) a bone and soft tissue malignancy is characterized by early metastasis to lung and bone [1]. Here we observed genes such as HOXD10, HOXD11 and HOXD13 normally involved in bone formation and ossification pattern of bones [22], to be HOXD locus including HOXD9 and HOXD12 where not uniquely up-regulated in primary ES compared to other tumors.…”
Section: Discussionmentioning
confidence: 68%
“…In search for factors presumably involved in their increased expression in ES we investigated putative ES originating cells such as neural crest or mesenchymal stem cells [1][2][3]. Though, genes of the HOXD locus were already expressed in mesenchymal or neural crest derived cells ( Figure 1B), they were not increased early after up-regulation of EWS-FLI1 in such stem cells nor did EWS-FLI1 knock down in ES lines influence HOXD10, HOXD11 or HOXD13 expression in vitro.…”
Section: Discussionmentioning
confidence: 99%
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“…[25][26][27][28] However, the addition of adjunctive, immune-activating therapies during first remission demonstrated the potential to reduce recurrence rates and exploit immunotherapy approaches for ES patients. 29 Balanced chromosomal EWS/ETS translocations that give rise to oncogenic chimeric proteins (EWS-ETS), the most common being EWS-FLI1 as a consequence of the t(11;22)(q24; q12) translocation, 30,31 are the characteristic driver event of ES tumorgenesis. 32 However, despite an MHC-class-II-restricted peptide derived from the fusion region of EWS-FLI1 that is able to initiate a CD4 C T-cell response, 33 no immunogenic ESspecific MHC-class-I-binding peptides derived from this fusion region have been identified, 34 prompting the search for further immunogenic epitopes of this disease.…”
Section: Discussionmentioning
confidence: 99%
“…1A). In Ewing's sarcoma, fusion oncogenes, generated by chromosome translocation, encode the N terminus of the EWS protein and the DNA-binding domains of ERG, FLI1, FEV, ETV1, or ETV4 (Mackintosh et al 2010). The difference between the prostate-and Ewing's sarcoma-related subsets of ETS proteins is likely due to the inclusion of the N terminus of EWS, which imparts novel transcriptional functions and is required for transformation (May et al 1993).…”
Section: Role Of Ets Genes In Other Cancersmentioning
confidence: 99%