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. 2022 Jul 29;21:156. doi: 10.1186/s12943-022-01628-3

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — The truncated tnFGFR1 shows a distinct profile of oncogenic signaling compared with the full length chimeric kinases. RPPA analysis of BaF3 cells transduced with either empty vector (MIG) or tnFGFR1 and maintained on IL3, or transformed with the BCR-FGFR1 chimeric kinase or its GZMB site mutated version (A). Selected preferentially activated pathways identified by RPPA are further validated by western blotting (B)