Article
The C-Terminal Kinase Domain-Binding and Suppression Motif Prevents Constitutive Activation of FGFR2.
Cancer research - 2 Sept 2025
Zingg Daniel, Lin Chi-Chuan, Yemelyanenko Julia, Wieteska Lukasz, Kas Sjors M, Bleijerveld Onno B, Chao Xue, Bhin Jinhyuk, Lutz Catrin, Wientjens Ellen, Klarenbeek Sjoerd, Zanetti Giulia, Annunziato Stefano, Siteur Bjørn, van der Burg Eline, Drenth Anne Paulien, van de Ven Marieke, Wessels Lodewyk F A, Altelaar Maarten, Ladbury John E, Jonkers Jos
Abstract excerpt
Genetic alterations in receptor tyrosine kinase genes can generate potent oncogenic drivers. Truncation of the FGFR2 gene by its last exon 18 (E18) is caused by structural alterations, such as focal amplifications and gene fusions/rearrangements, as well as by mutations. All the E18-truncating FGFR2 variants (FGFR2ΔE18) act as strong driver alterations in cancer, and they commonly encode a receptor lacking the...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
