FLI-1 gene

Watson DK, Smyth FE, Thompson DM, et al. The ERGB/FLI-1 gene Isolation and charactetization of a new member of the family of human ETS transctiption factors. Cell Growth Differ. 1992 3 705-713. 

Lelievre E, Lionneton F, Mattot V, et al. Ets-1 regulates ELIl expression in endothelial cells Identification of ETS binding sites in the FLI-1 gene promoter. J Biol Chem. 2002 277 25143-25151. 

A translocation involving the EWS gene on chromosome 22ql2 and other partners, most frequently the FLI-1 gene on chromosome Hq24, is typical for EWS/ PNET, and there are several different subtypes of EWS/ FLI-1 fusion transcripts. Other fusion partners... 

EWS/PNET has a variety of cytogenetic abnormalities involving the EWS gene, and the most common is a translocation involving chromosomes 11 and 22 with an EWS/ FLI-1 gene fusion. 

FLI-1 protein expression is typical for cases of EWS/PNET with a translocation involving the EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11, but nuclear FLI-1 reactivity is not entirely specific. 

Overexpression of the FLI-1 protein resulting from the translocation between the EWS and FLI-1 genes is observed in 71% to 100% of EWS/PNET, but the nuclear expression is not specific to the EWS/PNET group of tumors. In these circumstances, it is critical to include the clinical assessment of the patient along with other markers in the diagnostic panel. 

Landry JR, Konston S, Knezevic K, et al. FLI-1, EFLl, and ETSl r ulate the proximal promoter of the LM02 gene in endothelial cells. Blood. 2005 106 2680-2687. 

The FLI-1 protein is overexpressed in EWS/PNETs, which contain the EWS-FLIl/1 fusion gene, owing to the translocation t(ll 22)(q24 ql2). Nuclear FLI-1 immunoreactivity is found in approximately 70% of EWS/PNET but is also observed in nearly 90% of lymphoblastic lymphomas and in vascular tumors. TTs This antibody is useful as part of a panel for evaluation of potential EWS/PNET, when the overlap with lymphoblastic lymphomas and vascular neoplasms is considered. 

Fig. 1. Organization of fly and mouse Hox complexes. The eight fly Hox genes are diagrammed on top. The split between BX-C and ANT-C is indicated by a gap. The murine genes are given below, with cluster names on the left, and chromosome number in brackets. Orthologous genes are connected by vertical lines. The arrow indicates colinear Hox gene expression along the antero-posterior axis of flies and mice.

Despite these persuasive arguments, some recent observations oppose a strict EXD-switch. First, HOX proteins have been shown to activate transcription through sites that do not mediate co-operative DNA-binding with PBC members. Thus, an enhancer of the fly 1.28 gene is positively regulated by four DFD binding sites that do not permit co-operative association with EXD (Pederson et al., 2000). Because the activity of this enhancer was not examined in an exd null background, however, it is possible that EXD exerts an effect nonetheless. It could be proposed, therefore,... 

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