Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers

Understanding the mechanisms driving PI3K isoform dependency in prostate cancer can help the design of future clinical trials. Here, the authors show that gain-of-function mutations in PIK3CA or PIK3CB can confer PI3K p110 isoform dependency and that the direct inhibition of AKT may be superior to P...

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Autores principales:	Ninghui Mao, Zeda Zhang, Young Sun Lee, Danielle Choi, Aura Agudelo Rivera, Dan Li, Cindy Lee, Samuel Haywood, Xiaoping Chen, Qing Chang, Guotai Xu, Hsuan-An Chen, Elisa de Stanchina, Charles Sawyers, Neal Rosen, Andrew C. Hsieh, Yu Chen, Brett S. Carver
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/907e2e85e15748fa85c06a824495c169
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spelling	oai:doaj.org-article:907e2e85e15748fa85c06a824495c1692021-12-02T17:08:26ZDefining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers10.1038/s41467-021-25341-92041-1723https://doaj.org/article/907e2e85e15748fa85c06a824495c1692021-08-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-25341-9https://doaj.org/toc/2041-1723Understanding the mechanisms driving PI3K isoform dependency in prostate cancer can help the design of future clinical trials. Here, the authors show that gain-of-function mutations in PIK3CA or PIK3CB can confer PI3K p110 isoform dependency and that the direct inhibition of AKT may be superior to PI3K inhibition in PTEN-deficient prostate cancers.Ninghui MaoZeda ZhangYoung Sun LeeDanielle ChoiAura Agudelo RiveraDan LiCindy LeeSamuel HaywoodXiaoping ChenQing ChangGuotai XuHsuan-An ChenElisa de StanchinaCharles SawyersNeal RosenAndrew C. HsiehYu ChenBrett S. CarverNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Ninghui Mao Zeda Zhang Young Sun Lee Danielle Choi Aura Agudelo Rivera Dan Li Cindy Lee Samuel Haywood Xiaoping Chen Qing Chang Guotai Xu Hsuan-An Chen Elisa de Stanchina Charles Sawyers Neal Rosen Andrew C. Hsieh Yu Chen Brett S. Carver Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
description	Understanding the mechanisms driving PI3K isoform dependency in prostate cancer can help the design of future clinical trials. Here, the authors show that gain-of-function mutations in PIK3CA or PIK3CB can confer PI3K p110 isoform dependency and that the direct inhibition of AKT may be superior to PI3K inhibition in PTEN-deficient prostate cancers.
format	article
author	Ninghui Mao Zeda Zhang Young Sun Lee Danielle Choi Aura Agudelo Rivera Dan Li Cindy Lee Samuel Haywood Xiaoping Chen Qing Chang Guotai Xu Hsuan-An Chen Elisa de Stanchina Charles Sawyers Neal Rosen Andrew C. Hsieh Yu Chen Brett S. Carver
author_facet	Ninghui Mao Zeda Zhang Young Sun Lee Danielle Choi Aura Agudelo Rivera Dan Li Cindy Lee Samuel Haywood Xiaoping Chen Qing Chang Guotai Xu Hsuan-An Chen Elisa de Stanchina Charles Sawyers Neal Rosen Andrew C. Hsieh Yu Chen Brett S. Carver
author_sort	Ninghui Mao
title	Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
title_short	Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
title_full	Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
title_fullStr	Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
title_full_unstemmed	Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers
title_sort	defining the therapeutic selective dependencies for distinct subtypes of pi3k pathway-altered prostate cancers
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/907e2e85e15748fa85c06a824495c169
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Defining the therapeutic selective dependencies for distinct subtypes of PI3K pathway-altered prostate cancers

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