Open Access Viewpoints

WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?

Nicolas Gillet1,2†, Alexandre Carpentier1,2, Pierre-Yves Barez1,2 and Luc Willems1,2*

Author Affiliations

1 Molecular and Cellular Epigenetics, GIGA, University of Liège, Liège, Belgium

2 Molecular biology, GxABT, University of Liège, Gembloux, Belgium

For all author emails, please log on.

Retrovirology 2012, 9:115 doi:10.1186/1742-4690-9-115

Published: 21 December 2012

Abstract

Attenuation of p53 activity appears to be a major step in Human T-lymphotropic virus type 1 (HTLV-1) Tax transformation. However, p53 genomic mutations are late and rather infrequent events in HTLV-1 induced Adult T cell leukemia (ATL). The paper by Zane et al. shows that a mediator of p53 activity, Wild-type p53-induced phosphatase 1 (Wip1), contributes to Tax-induced oncogenesis in a mouse model. Wip1 may therefore be a novel target for therapeutic approaches.

Keywords:
HTLV-1; Tax; HBZ; p53; Wip1; PPM1D; MDM2; DNA damage response; Genomic stress; ATM; Chk2