title: WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
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.
authors.affiliation: Molecular and Cellular Epigenetics, GIGA, University of Liège, Liège, Belgium.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Gillet
authors.forename: Alexandre
authors.initials: A
authors.lastname: Carpentier
authors.forename: Pierre-Yves
authors.initials: PY
authors.lastname: Barez
authors.forename: Luc
authors.initials: L
authors.lastname: Willems
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D002472:Cell Transformation, Viral; D016356:Gene Products, tax / Q000378:metabolism*; D006801:Humans; D010749:Phosphoprotein Phosphatases / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D016356:Gene Products, tax; D016159:Tumor Suppressor Protein p53; D010749:Phosphoprotein Phosphatases