TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma

Pre-clinical studies have shown that TP53 mutations can account for acquired resistance to HDM2 antagonists. This study provides clinical evidence for the emergence of TP53mutations in circulating cell-free DNA, seen in 5 out of 20 de-differentiated liposarcoma patients treated with an HDM2 antagoni...

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Autores principales: Joonil Jung, Joon Sang Lee, Mark A. Dickson, Gary K. Schwartz, Axel Le Cesne, Andrea Varga, Rastilav Bahleda, Andrew J. Wagner, Edwin Choy, Maja J. de Jonge, Madelyn Light, Steve Rowley, Sandrine Macé, James Watters
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Publicado: Nature Portfolio 2016
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Acceso en línea:https://doaj.org/article/260fdcaadef641d3801dbcc9cba2ac83
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spelling oai:doaj.org-article:260fdcaadef641d3801dbcc9cba2ac832021-12-02T14:38:36ZTP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma10.1038/ncomms126092041-1723https://doaj.org/article/260fdcaadef641d3801dbcc9cba2ac832016-08-01T00:00:00Zhttps://doi.org/10.1038/ncomms12609https://doaj.org/toc/2041-1723Pre-clinical studies have shown that TP53 mutations can account for acquired resistance to HDM2 antagonists. This study provides clinical evidence for the emergence of TP53mutations in circulating cell-free DNA, seen in 5 out of 20 de-differentiated liposarcoma patients treated with an HDM2 antagonist.Joonil JungJoon Sang LeeMark A. DicksonGary K. SchwartzAxel Le CesneAndrea VargaRastilav BahledaAndrew J. WagnerEdwin ChoyMaja J. de JongeMadelyn LightSteve RowleySandrine MacéJames WattersNature PortfolioarticleScienceQENNature Communications, Vol 7, Iss 1, Pp 1-7 (2016)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Joonil Jung
Joon Sang Lee
Mark A. Dickson
Gary K. Schwartz
Axel Le Cesne
Andrea Varga
Rastilav Bahleda
Andrew J. Wagner
Edwin Choy
Maja J. de Jonge
Madelyn Light
Steve Rowley
Sandrine Macé
James Watters
TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
description Pre-clinical studies have shown that TP53 mutations can account for acquired resistance to HDM2 antagonists. This study provides clinical evidence for the emergence of TP53mutations in circulating cell-free DNA, seen in 5 out of 20 de-differentiated liposarcoma patients treated with an HDM2 antagonist.
format article
author Joonil Jung
Joon Sang Lee
Mark A. Dickson
Gary K. Schwartz
Axel Le Cesne
Andrea Varga
Rastilav Bahleda
Andrew J. Wagner
Edwin Choy
Maja J. de Jonge
Madelyn Light
Steve Rowley
Sandrine Macé
James Watters
author_facet Joonil Jung
Joon Sang Lee
Mark A. Dickson
Gary K. Schwartz
Axel Le Cesne
Andrea Varga
Rastilav Bahleda
Andrew J. Wagner
Edwin Choy
Maja J. de Jonge
Madelyn Light
Steve Rowley
Sandrine Macé
James Watters
author_sort Joonil Jung
title TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
title_short TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
title_full TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
title_fullStr TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
title_full_unstemmed TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma
title_sort tp53 mutations emerge with hdm2 inhibitor sar405838 treatment in de-differentiated liposarcoma
publisher Nature Portfolio
publishDate 2016
url https://doaj.org/article/260fdcaadef641d3801dbcc9cba2ac83
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