Translocation involving chromosome 22 in Ewing's Sarcoma. A cytogenetic study of four fresh tumors

Aurias, Alain; C, Rimbaut; Buffe, D; Zucker, Jean‐Michel; Mazabraud, A

doi:10.1016/0165-4608(84)90003-7

Cited by 206 publications

(95 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Translocations of 9q34 with 22q11-13 are known to be not limited to CML and ALL, and have been reported in several solid tumors where it often a frequent, recurring event These include oral squamous cell carcinona [43], lung carcinoma [44], lipoma [45], retinoblastoma [46], osteosarcoma [47], chondrosarcoma [48], and Ewing's sarcoma [49] Li-Fraumeni cells passaged in tissue culture recurrently select for translocations of the same regions after long term passage [50]. With the highly complex karyotypes of most solid tumors, little attention has been paid to the 9;22 translocation in these other systems.…”

Section: Discussionmentioning

confidence: 99%

aCGH local copy number aberrations associated with overall copy number genomic instability in colorectal cancer: Coordinate involvement of the regions including BCR and ABL

Bartos

Gaile

McQuaid

et al. 2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

View full text Add to dashboard Cite

In order to identify small regions of the genome whose specific copy number alteration is associated with high genomic instability in the form of overall genome-wide copy number aberrations, we have analyzed array-based comparative genomic hybridization (aCGH) data from 33 sporadic colorectal carcinomas. Copy number changes of a small number of specific regions were significantly correlated with elevated overall amplifications and deletions scattered throughout the entire genome. One significant region at 9q34 includes the c-ABL gene Another region spanning 22q11-13 includes the breakpoint cluster region (BCR) of the Philadelphia chromosome Coordinate 22q11-13 alterations were observed in nine of eleven tumors with the 9q34 alteration Additional regions on 1q and 14q were associated with overall genome-wide copy number changes, while copy number aberrations on chromosome 7p, 7q, and 13q21.1-31.3 were found associated with this instability only in tumors from patients with a smoking history Our analysis demonstrates there are a small number of regions of the genome where gain or loss is commonly associated with a tumor's overall level of copy number aberrations Our finding BCR and ABL located within two of the instability-associated regions, and the involvement of these two regions occurring coordinately, suggests a system akin to the BCR-ABL translocation of CML may be involved in genomic instability in about one-third of human colorectal carcinomas.

show abstract

Section: Discussionmentioning

confidence: 99%

aCGH local copy number aberrations associated with overall copy number genomic instability in colorectal cancer: Coordinate involvement of the regions including BCR and ABL

Bartos

Gaile

McQuaid

et al. 2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

View full text Add to dashboard Cite

show abstract

“…Their genetic hallmark is the presence of the reciprocal t(11;22)(q24;q12) translocation (Aurias et al, 1984;Mugneret et al, 1988), or other less frequent variant translocations t(21;22)(q12;q12) and t(7;22)(p22;q12), and their morphology falls in the smallblue-round-cells category. The t(11;22) translocation leads to the fusion of the EWS gene on 22q12 with the FLI1 gene on 11q24, resulting in the formation and expression of the chimaeric transcript EWS-FLI1 (Delattre et al, 1992) that is thought to contribute to the pathogenesis of this tumour by modulating the expression of target genes.…”

Section: Introductionmentioning

confidence: 99%

Array CGH and gene-expression profiling reveals distinct genomic instability patterns associated with DNA repair and cell-cycle checkpoint pathways in Ewing's sarcoma

et al. 2007

View full text Add to dashboard Cite

“…In many cases gene rearrangements associated with these neoplasms result in structural alteration of transcription factors (Rabbitts, 1994). The t(11;22)(q24;q12) translocation observed in 85% of the Ewing family of tumors (ET), results in fusion of the EWS gene with the ets family transcription factor gene Fli1 (Turc Carel et al, 1983;Delattre et al, 1992;Aurias et al, 1983). The EWS-Fli1 fusion gene codes for a chimeric protein in which the amino terminal moiety of EWS, which is rich in glutamine, serine and tyrosine residues, is fused to the carboxy-terminal DNA-binding domain (ets domain) of Fli1 (Delattre et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Oncogenic EWS-Fli1 interacts with hsRPB7, a subunit of human RNA polymerase II

et al. 1998

View full text Add to dashboard Cite

As a result of the t(11;22)(q24;q12) chromosomal translocation characterizing the Ewing family of tumors (ET), the amino terminal portion of EWS, an RNA binding protein of unknown function, is fused to the DNA-binding domain of the ets transcription factor Fli1. The hybrid EWS-Fli1 protein acts as a strong transcriptional activator and, in contrast to wildtype Fli1, is a potent transforming agent. Similar rearrangements involving EWS or the highly homologous TLS with various transcription factors have been found in several types of human tumors. Employing yeast twohybrid cloning we isolated the seventh largest subunit of human RNA polymerase II (hsRPB7) as a protein that speci®cally interacts with the amino terminus of EWS. This association was con®rmed by in vitro immunocoprecipitation. In nuclear extracts, hsRPB7 was found to copurify with EWS-Fli1 but not with Fli1. Overexpression of recombinant hsRPB7 speci®cally increased gene activation by EWS-chimeric transcription factors. Replacement of the EWS portion by hsRPB7 in the oncogenic fusion protein restored the transactivating potential of the chimera. Our results suggest that the interaction of the amino terminus of EWS with hsRPB7 contributes to the transactivation function of EWS-Fli1 and, since hsRPB7 has characteristics of a regulatory subunit of RNA polymerase II, may in¯uence promoter selectivity.

show abstract

Translocation involving chromosome 22 in Ewing's Sarcoma. A cytogenetic study of four fresh tumors

Cited by 206 publications

References 6 publications

aCGH local copy number aberrations associated with overall copy number genomic instability in colorectal cancer: Coordinate involvement of the regions including BCR and ABL

aCGH local copy number aberrations associated with overall copy number genomic instability in colorectal cancer: Coordinate involvement of the regions including BCR and ABL

Array CGH and gene-expression profiling reveals distinct genomic instability patterns associated with DNA repair and cell-cycle checkpoint pathways in Ewing's sarcoma

Oncogenic EWS-Fli1 interacts with hsRPB7, a subunit of human RNA polymerase II

Contact Info

Product

Resources

About