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

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,...

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Detalles Bibliográficos
Autores principales: Gillet, Nicolas, Carpentier, Alexandre, Barez, Pierre-Yves, Willems, Luc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Viewpoints
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3542286/
https://www.ncbi.nlm.nih.gov/pubmed/23256570
http://dx.doi.org/10.1186/1742-4690-9-115
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author Gillet, Nicolas
Carpentier, Alexandre
Barez, Pierre-Yves
Willems, Luc
author_facet Gillet, Nicolas
Carpentier, Alexandre
Barez, Pierre-Yves
Willems, Luc
author_sort Gillet, Nicolas
collection PubMed
description 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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spelling pubmed-35422862013-01-11 WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL? Gillet, Nicolas Carpentier, Alexandre Barez, Pierre-Yves Willems, Luc Retrovirology Viewpoints 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. BioMed Central 2012-12-21 /pmc/articles/PMC3542286/ /pubmed/23256570 http://dx.doi.org/10.1186/1742-4690-9-115 Text en Copyright ©2012 Gillet et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Viewpoints
Gillet, Nicolas
Carpentier, Alexandre
Barez, Pierre-Yves
Willems, Luc
WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title_full WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title_fullStr WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title_full_unstemmed WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title_short WIP1 deficiency inhibits HTLV-1 Tax oncogenesis: novel therapeutic prospects for treatment of ATL?
title_sort wip1 deficiency inhibits htlv-1 tax oncogenesis: novel therapeutic prospects for treatment of atl?
topic Viewpoints
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3542286/
https://www.ncbi.nlm.nih.gov/pubmed/23256570
http://dx.doi.org/10.1186/1742-4690-9-115
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AT barezpierreyves wip1deficiencyinhibitshtlv1taxoncogenesisnoveltherapeuticprospectsfortreatmentofatl
AT willemsluc wip1deficiencyinhibitshtlv1taxoncogenesisnoveltherapeuticprospectsfortreatmentofatl

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