Literature DB >> 18521227

Progress in the molecular biology of ewing tumors.

H Kovar1.   

Abstract

Purpose/results/discussion. Rearrangement of the EWS gene with an ETS oncogene by chromosomal translocation is a hallmark of the Ewing family of tumors (EFT). Detectability, incidence, tumor specificity and variability of this aberration have been matters of intense investigation in recent years. A number of related alterations have also been found in other malignancies. The common consequence of these gene rearrangements is the generation of an aberrant transcription factor. In EFT, the ETS partner is responsible for target recognition. However, synergistic and possibly tissue-restricted transcription factors interacting with either the EWS or the ETS portion may influence target selection. Minimal domains of both fusion partners were defined that have proved necessary for the in vitro transformation of murine fibroblasts. These functional studies suggest a role for aberrant transcriptional regulation of transforming target genes by the chimeric transcription factors. Also, fusion of the two unrelated protein domains may affect overall protein conformation and consequently DNA binding specificity. Recent evidence suggests that EWS, when fused to a transcription factor, interacts with different partners than germ-line EWS. Variability in EWS-ETS gene fusions has recently been demonstrated to correlate with clinical outcome. This finding may reflect functional differences of the individual chimeric transcription factors. Alternatively, type and availability of specific recombinases at different time-points of stem cell development or in different stem cell lineages may determine fusion type. Studies on EFT cell lines using EWS-ETS antagonists do suggest a rate-limiting essential role for the gene rearrangement in the self-renewal capacity of EFT cells. The presence of additional aberrations varying in number and type that may account for immortalization and full transformation is postulated. Knowledge about such secondary alterations may provide valuable prognostic markers that could be used for treatment stratification.

Entities:  

Year:  1998        PMID: 18521227      PMCID: PMC2395372          DOI: 10.1080/13577149878109

Source DB:  PubMed          Journal:  Sarcoma        ISSN: 1357-714X


  123 in total

1.  A novel chimera gene between EWS and E1A-F, encoding the adenovirus E1A enhancer-binding protein, in extraosseous Ewing's sarcoma.

Authors:  F Urano; A Umezawa; W Hong; H Kikuchi; J Hata
Journal:  Biochem Biophys Res Commun       Date:  1996-02-15       Impact factor: 3.575

2.  Solution structure of the ETS domain from murine Ets-1: a winged helix-turn-helix DNA binding motif.

Authors:  L W Donaldson; J M Petersen; B J Graves; L P McIntosh
Journal:  EMBO J       Date:  1996-01-02       Impact factor: 11.598

3.  Ewing sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation.

Authors:  W A May; M L Gishizky; S L Lessnick; L B Lunsford; B C Lewis; O Delattre; J Zucman; G Thomas; C T Denny
Journal:  Proc Natl Acad Sci U S A       Date:  1993-06-15       Impact factor: 11.205

4.  The solution structure of the human ETS1-DNA complex reveals a novel mode of binding and true side chain intercalation.

Authors:  M H Werner; M Clore; C L Fisher; R J Fisher; L Trinh; J Shiloach; A M Gronenborn
Journal:  Cell       Date:  1995-12-01       Impact factor: 41.582

5.  Fusion of the EWS gene to CHN, a member of the steroid/thyroid receptor gene superfamily, in a human myxoid chondrosarcoma.

Authors:  J Clark; H Benjamin; S Gill; S Sidhar; G Goodwin; J Crew; B A Gusterson; J Shipley; C S Cooper
Journal:  Oncogene       Date:  1996-01-18       Impact factor: 9.867

6.  A single ets-related transcription factor, E1AF, confers invasive phenotype on human cancer cells.

Authors:  M Kaya; K Yoshida; F Higashino; T Mitaka; S Ishii; K Fujinaga
Journal:  Oncogene       Date:  1996-01-18       Impact factor: 9.867

7.  Olfactory neuroblastoma is a peripheral primitive neuroectodermal tumor related to Ewing sarcoma.

Authors:  P H Sorensen; J K Wu; K W Berean; J F Lim; W Donn; H F Frierson; C P Reynolds; D López-Terrada; T J Triche
Journal:  Proc Natl Acad Sci U S A       Date:  1996-02-06       Impact factor: 11.205

8.  SRE elements are binding sites for the fusion protein EWS-FLI-1.

Authors:  L Magnaghi-Jaulin; H Masutani; P Robin; M Lipinski; A Harel-Bellan
Journal:  Nucleic Acids Res       Date:  1996-03-15       Impact factor: 16.971

9.  International variations in the incidence of childhood bone tumours.

Authors:  D M Parkin; C A Stiller; J Nectoux
Journal:  Int J Cancer       Date:  1993-02-01       Impact factor: 7.396

10.  Fusion of CHOP to a novel RNA-binding protein in human myxoid liposarcoma.

Authors:  A Crozat; P Aman; N Mandahl; D Ron
Journal:  Nature       Date:  1993-06-17       Impact factor: 49.962

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  4 in total

1.  Association of EWS-FLI1 type 1 fusion with lower proliferative rate in Ewing's sarcoma.

Authors:  E de Alava; A Panizo; C R Antonescu; A G Huvos; F J Pardo-Mindán; F G Barr; M Ladanyi
Journal:  Am J Pathol       Date:  2000-03       Impact factor: 4.307

2.  Specific recognition and inhibition of Ewing tumour growth by antigen-specific allo-restricted cytotoxic T cells.

Authors:  U Thiel; S Pirson; C Müller-Spahn; H Conrad; D H Busch; H Bernhard; S Burdach; G H S Richter
Journal:  Br J Cancer       Date:  2011-03-15       Impact factor: 7.640

3.  Detection of EWS/FLI-1 by Immunostaining. An Adjunctive Tool in Diagnosis of Ewing's Sarcoma and Primitive Neuroectodermal Tumour on Cytological Samples and Paraffin-Embedded Archival Material.

Authors:  G Nilsson; M Wang; J Wejde; A Kreicbergs; O Larsson
Journal:  Sarcoma       Date:  1999

4.  Molecular approaches to sarcoma therapy.

Authors:  R J Olsen; S R Tarantolo; S H Hinrichs
Journal:  Sarcoma       Date:  2002
  4 in total

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