This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kovar, H. Articles by Hoeben, R. C. Search for Related Content PubMed PubMed Citation Articles by Kovar, H. Articles by Hoeben, R. C.

Adenovirus E1A Does Not Induce the Ewing Tumor-associated Gene Fusion EWS-FLI1¹

Children’s Cancer Research Institute, St. Anna Kinderspital, A-1090 Vienna, Austria [H. K., I. P., D. J., S. B., P. F. A., D. N. T. A.], and Department of Molecular Cell Biology, Leiden University Medical Centre, 2333 AL Leiden, the Netherlands [F. J. F., J. C. A. G. W., R. C. H.]

Rearrangement of the EWS gene with FLI1 is thought to occur early in the pathogenesis of Ewing’s sarcoma family tumors (EFTs) because the chromosomal aberration is pathognomonic for this disease. Recently, adenovirus (Ad) 5 E1A protein has been reported to induce this gene rearrangement in a variety of cell types. This finding, if generally substantiated, not only suggests an etiological role for viral agents in the generation of oncogenic chromosomal aberrations but would also significantly impact the use of adenoviral vectors for gene therapy. In contrast, we now report on the absence of EWS-FLI1 chimeric products from short- and long-term cultures of stably Ad-transformed cells lines and from transiently E1A-expressing cell lines. In addition, we demonstrate the absence of E1A from EFTs. We conclude that there is no role for Ads in EFT pathogenesis. Consequently, evidence for a viral genesis of tumor-specific gene rearrangements is not available.

This article has been cited by other articles:

				F. Meric, Y. Liao, W.-P. Lee, R. E. Pollock, and M.-C. Hung Adenovirus 5 Early Region 1A Does Not Induce Expression of the Ewing Sarcoma Fusion Product EWS-FLI1 in Breast and Ovarian Cancer Cell Lines Clin. Cancer Res., October 1, 2000; 6(10): 3832 - 3836. [Abstract] [Full Text]