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E1A and the Ewing tumor translocation

Nature Medicine volume 5, page 1331 (1999)Cite this article

To the editor—Breakpoint variation and the resulting fusion type heterogeneity are characteristic of the Ewing tumor-associated EWS–FLI1 gene rearrangement. Sanchez-Prieto et al. report high efficiency induction of EWS–FLI1recombination in a variety of cell types by adenovirus E1A (ref 1). To our surprise, only a single fusion transcript type (type 1 or type 2) was found in individual E1A transfections, instead of the expected polyclonal rearrangement. To characterize the E1A-induced gene fusions in more detail, we sought to repeat the experiments described by Sanchez-Prieto et al.

Adenovirus 5 E1A was expressed from a CMV promoter in HeLa cervix carcinoma cells, a human fibroblast cell line and a neuroblastoma cell line after lipofection. Transfection efficiencies were approximately 2%, 4% and 80%, respectively. We used a one-tube nested PCR approach capable of identifying one EWS–FLI1-expressing cell in a total of 106 cells6 to screen for expression of the Ewing tumor specific gene rearrangement 70 hours after transfection. No EWS–FLI1 transcript was detectable in any of the transiently E1A-transfected cells, although E1A expression was confirmed.

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References

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  1. CCRI St. Anna Kinderspital, Kinderspitalgasse 6, Vienna, A-1090, Austria

    Heinrich Kovar

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  1. Heinrich Kovar
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Kovar, H. E1A and the Ewing tumor translocation. Nat Med 5, 1331 (1999). https://doi.org/10.1038/70880

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