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

被引:0
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作者
Nicolas Gillet
Alexandre Carpentier
Pierre-Yves Barez
Luc Willems
机构
[1] University of Liège,Molecular and Cellular Epigenetics, GIGA
[2] University of Liège,Molecular biology, GxABT
来源
Retrovirology | / 9卷
关键词
HTLV-1; Tax; HBZ; p53; Wip1; PPM1D; MDM2; DNA damage response; Genomic stress; ATM; Chk2;
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摘要
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.
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