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Brief Report
DEK Expression is Controlled by E2F and Deregulated in Diverse Tumor Type
Maria Stella Carro, Fabio Mario Spiga, Micaela Quarto, Valentina Di Ninni, Sara Volorio, Myriam Alcalay and Heiko Müller
volume 5 | issue 11
1 june 2006Pages: 1202 - 1207
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Deregulation of the retinoblastoma (pRB) tumor suppressor pathway associated with
aberrant activity of E2F transcription factors is frequently observed in human cancer.
Microarray based analyses have revealed a large number of potential downstream
mediators of the tumor suppressing activity of pRB, including DEK, a fusion partner of
CAN found in a subset of acute myeloid leukaemia (AML) patients carrying a (6; 9)
translocation.
Here we report that the expression of DEK is under direct control of E2F transcription
factors. Chromatin immunoprecipitation assays show that the DEK promoter is bound by
endogenous E2F in vivo. The DEK promoter is transactivated by E2F and mutation of
E2F binding sites eliminates this effect. Expression levels of DEK in human tumors have
been investigated by tissue micro array analysis. We find that DEK is overexpressed in
many solid tumors such as colon cancer, larynx cancer, bladder cancer, and melanoma.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.