Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer

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
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Science
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Acceso en línea:https://doaj.org/article/9657645615f24b61be1f24096a3bc13c
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Sumario: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.

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