Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer

Cancer subtypes may have distinct metabolic vulnerabilities that can be exploited for therapeutic interventions. Here, the authors show that in lung cancer, genetic activation of distinct oncogenic receptor tyrosine kinases results in unique metabolic liabilities and, in particular, EGFR aberrant ca...

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Autores principales: Nan Jin, Aiwei Bi, Xiaojing Lan, Jun Xu, Xiaomin Wang, Yingluo Liu, Ting Wang, Shuai Tang, Hanlin Zeng, Ziqi Chen, Minjia Tan, Jing Ai, Hua Xie, Tao Zhang, Dandan Liu, Ruimin Huang, Yue Song, Elaine Lai-Han Leung, Xiaojun Yao, Jian Ding, Meiyu Geng, Shu-Hai Lin, Min Huang
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Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/9657645615f24b61be1f24096a3bc13c
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spelling oai:doaj.org-article:9657645615f24b61be1f24096a3bc13c2021-12-02T17:01:29ZIdentification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer10.1038/s41467-019-10427-22041-1723https://doaj.org/article/9657645615f24b61be1f24096a3bc13c2019-06-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-10427-2https://doaj.org/toc/2041-1723Cancer subtypes may have distinct metabolic vulnerabilities that can be exploited for therapeutic interventions. Here, the authors show that in lung cancer, genetic activation of distinct oncogenic receptor tyrosine kinases results in unique metabolic liabilities and, in particular, EGFR aberrant cancers rely on the serine biosynthetic pathway while FGFR aberrant cancers rely on glycolysis.Nan JinAiwei BiXiaojing LanJun XuXiaomin WangYingluo LiuTing WangShuai TangHanlin ZengZiqi ChenMinjia TanJing AiHua XieTao ZhangDandan LiuRuimin HuangYue SongElaine Lai-Han LeungXiaojun YaoJian DingMeiyu GengShu-Hai LinMin HuangNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-15 (2019)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Nan Jin
Aiwei Bi
Xiaojing Lan
Jun Xu
Xiaomin Wang
Yingluo Liu
Ting Wang
Shuai Tang
Hanlin Zeng
Ziqi Chen
Minjia Tan
Jing Ai
Hua Xie
Tao Zhang
Dandan Liu
Ruimin Huang
Yue Song
Elaine Lai-Han Leung
Xiaojun Yao
Jian Ding
Meiyu Geng
Shu-Hai Lin
Min Huang
Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
description Cancer subtypes may have distinct metabolic vulnerabilities that can be exploited for therapeutic interventions. Here, the authors show that in lung cancer, genetic activation of distinct oncogenic receptor tyrosine kinases results in unique metabolic liabilities and, in particular, EGFR aberrant cancers rely on the serine biosynthetic pathway while FGFR aberrant cancers rely on glycolysis.
format article
author Nan Jin
Aiwei Bi
Xiaojing Lan
Jun Xu
Xiaomin Wang
Yingluo Liu
Ting Wang
Shuai Tang
Hanlin Zeng
Ziqi Chen
Minjia Tan
Jing Ai
Hua Xie
Tao Zhang
Dandan Liu
Ruimin Huang
Yue Song
Elaine Lai-Han Leung
Xiaojun Yao
Jian Ding
Meiyu Geng
Shu-Hai Lin
Min Huang
author_facet Nan Jin
Aiwei Bi
Xiaojing Lan
Jun Xu
Xiaomin Wang
Yingluo Liu
Ting Wang
Shuai Tang
Hanlin Zeng
Ziqi Chen
Minjia Tan
Jing Ai
Hua Xie
Tao Zhang
Dandan Liu
Ruimin Huang
Yue Song
Elaine Lai-Han Leung
Xiaojun Yao
Jian Ding
Meiyu Geng
Shu-Hai Lin
Min Huang
author_sort Nan Jin
title Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
title_short Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
title_full Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
title_fullStr Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
title_full_unstemmed Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
title_sort identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/9657645615f24b61be1f24096a3bc13c
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