The EWS protein is dispensable for Ewing tumor growth

H. Kovar, G. Jug, C. Hattinger, L. Spahn, D. N T Aryee, P. F. Ambros, A. Zoubek, H. Gadner

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

EWS encodes a ubiquitously expressed RNA binding protein with largely unknown function. In Ewing sarcoma family tumors (EFT), one allele is rearranged with an ETS gene. This is the first description of an EFT with a complete EWS deficiency in the presence of two copies of a rearranged chromosome 22 carrying an interstitial EWS-FL11 translocation. Absence of EWS protein suggested that it is dispensable for EFT growth. By sequencing of EWS cDNA from unrelated EFTs, we excluded inactivation of EWS as a general mechanism in EFT pathogenesis. Rather, EWS was found to be uniformly expressed in two splicing variants of similar abundaney, EWSα and EWSβ, which differ in a single amino acid. Three EWS negative cell lines were established, which will serve as valuable models to study normal and aberrant EWS function upon reintroduction into the tumor cells.

Original languageEnglish
Pages (from-to)5992-5997
Number of pages6
JournalCancer Research
Volume61
Issue number16
Publication statusPublished - Aug 15 2001

Fingerprint

RNA-Binding Protein EWS
Ewing's Sarcoma
Growth
Neoplasms
Chromosomes, Human, Pair 22
RNA-Binding Proteins
Complementary DNA
Alleles
Amino Acids
Cell Line
Genes

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Kovar, H., Jug, G., Hattinger, C., Spahn, L., Aryee, D. N. T., Ambros, P. F., ... Gadner, H. (2001). The EWS protein is dispensable for Ewing tumor growth. Cancer Research, 61(16), 5992-5997.

The EWS protein is dispensable for Ewing tumor growth. / Kovar, H.; Jug, G.; Hattinger, C.; Spahn, L.; Aryee, D. N T; Ambros, P. F.; Zoubek, A.; Gadner, H.

In: Cancer Research, Vol. 61, No. 16, 15.08.2001, p. 5992-5997.

Research output: Contribution to journalArticle

Kovar, H, Jug, G, Hattinger, C, Spahn, L, Aryee, DNT, Ambros, PF, Zoubek, A & Gadner, H 2001, 'The EWS protein is dispensable for Ewing tumor growth', Cancer Research, vol. 61, no. 16, pp. 5992-5997.
Kovar H, Jug G, Hattinger C, Spahn L, Aryee DNT, Ambros PF et al. The EWS protein is dispensable for Ewing tumor growth. Cancer Research. 2001 Aug 15;61(16):5992-5997.
Kovar, H. ; Jug, G. ; Hattinger, C. ; Spahn, L. ; Aryee, D. N T ; Ambros, P. F. ; Zoubek, A. ; Gadner, H. / The EWS protein is dispensable for Ewing tumor growth. In: Cancer Research. 2001 ; Vol. 61, No. 16. pp. 5992-5997.
@article{148d9c201fe44da4b8756ccbc2c04d25,
title = "The EWS protein is dispensable for Ewing tumor growth",
abstract = "EWS encodes a ubiquitously expressed RNA binding protein with largely unknown function. In Ewing sarcoma family tumors (EFT), one allele is rearranged with an ETS gene. This is the first description of an EFT with a complete EWS deficiency in the presence of two copies of a rearranged chromosome 22 carrying an interstitial EWS-FL11 translocation. Absence of EWS protein suggested that it is dispensable for EFT growth. By sequencing of EWS cDNA from unrelated EFTs, we excluded inactivation of EWS as a general mechanism in EFT pathogenesis. Rather, EWS was found to be uniformly expressed in two splicing variants of similar abundaney, EWSα and EWSβ, which differ in a single amino acid. Three EWS negative cell lines were established, which will serve as valuable models to study normal and aberrant EWS function upon reintroduction into the tumor cells.",
author = "H. Kovar and G. Jug and C. Hattinger and L. Spahn and Aryee, {D. N T} and Ambros, {P. F.} and A. Zoubek and H. Gadner",
year = "2001",
month = "8",
day = "15",
language = "English",
volume = "61",
pages = "5992--5997",
journal = "Journal of Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "16",

}

TY - JOUR

T1 - The EWS protein is dispensable for Ewing tumor growth

AU - Kovar, H.

AU - Jug, G.

AU - Hattinger, C.

AU - Spahn, L.

AU - Aryee, D. N T

AU - Ambros, P. F.

AU - Zoubek, A.

AU - Gadner, H.

PY - 2001/8/15

Y1 - 2001/8/15

N2 - EWS encodes a ubiquitously expressed RNA binding protein with largely unknown function. In Ewing sarcoma family tumors (EFT), one allele is rearranged with an ETS gene. This is the first description of an EFT with a complete EWS deficiency in the presence of two copies of a rearranged chromosome 22 carrying an interstitial EWS-FL11 translocation. Absence of EWS protein suggested that it is dispensable for EFT growth. By sequencing of EWS cDNA from unrelated EFTs, we excluded inactivation of EWS as a general mechanism in EFT pathogenesis. Rather, EWS was found to be uniformly expressed in two splicing variants of similar abundaney, EWSα and EWSβ, which differ in a single amino acid. Three EWS negative cell lines were established, which will serve as valuable models to study normal and aberrant EWS function upon reintroduction into the tumor cells.

AB - EWS encodes a ubiquitously expressed RNA binding protein with largely unknown function. In Ewing sarcoma family tumors (EFT), one allele is rearranged with an ETS gene. This is the first description of an EFT with a complete EWS deficiency in the presence of two copies of a rearranged chromosome 22 carrying an interstitial EWS-FL11 translocation. Absence of EWS protein suggested that it is dispensable for EFT growth. By sequencing of EWS cDNA from unrelated EFTs, we excluded inactivation of EWS as a general mechanism in EFT pathogenesis. Rather, EWS was found to be uniformly expressed in two splicing variants of similar abundaney, EWSα and EWSβ, which differ in a single amino acid. Three EWS negative cell lines were established, which will serve as valuable models to study normal and aberrant EWS function upon reintroduction into the tumor cells.

UR - http://www.scopus.com/inward/record.url?scp=0035881569&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035881569&partnerID=8YFLogxK

M3 - Article

VL - 61

SP - 5992

EP - 5997

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0008-5472

IS - 16

ER -