Rewiring ERBB3 and ERK signaling confers resistance to FGFR1 inhibition in gastrointestinal cancer harbored an ERBB3-E928G mutation

Protein Cell. 2020 Dec;11(12):915-920. doi: 10.1007/s13238-020-00749-z.

Authors

Xiang Yang¹, Hongxiao Wang¹, Enjun Xie¹, Biyao Tang¹, Qingdian Mu¹, Zijun Song¹, Junyi Chen¹, Fudi Wang¹, Junxia Min²

Affiliations

¹ The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, 310058, China.
² The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, 310058, China. junxiamin@zju.edu.cn.

No abstract available

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Amino Acid Substitution
Antineoplastic Agents / pharmacology*
Cell Line, Tumor
Drug Resistance, Neoplasm* / drug effects
Drug Resistance, Neoplasm* / genetics
Gastrointestinal Neoplasms* / genetics
Gastrointestinal Neoplasms* / metabolism
Gastrointestinal Neoplasms* / pathology
Humans
MAP Kinase Signaling System* / drug effects
MAP Kinase Signaling System* / genetics
Mutation, Missense*
Receptor, ErbB-3* / genetics
Receptor, ErbB-3* / metabolism
Receptor, Fibroblast Growth Factor, Type 1* / antagonists & inhibitors
Receptor, Fibroblast Growth Factor, Type 1* / genetics
Receptor, Fibroblast Growth Factor, Type 1* / metabolism

Substances

Antineoplastic Agents
ERBB3 protein, human
FGFR1 protein, human
Receptor, ErbB-3
Receptor, Fibroblast Growth Factor, Type 1