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

Retrovirology. 2012 Dec 21:9:115. doi: 10.1186/1742-4690-9-115.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic / metabolism*
  • Cell Transformation, Viral*
  • Gene Products, tax / metabolism*
  • Humans
  • Phosphoprotein Phosphatases / metabolism*
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Gene Products, tax
  • Tumor Suppressor Protein p53
  • Phosphoprotein Phosphatases