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A study addressing why the IGF-1R pathway silencing through IGF-1R fusion protein IGF-Trap-induced IGF-1/2 bioavailability reduction, which was a promising anticancer strategy in vitro failed in nude mice xenotransplanted with the human triple negative breast cancer MDA-MB-231 cells, found that these cells developed resistance to IGF-targeted therapy by increasing the activation of another receptor tyrosine kinase, fibroblast growth factor receptor 1 (FGFR1) (75)

10.1016/j.jalz.2013.12.015 [DOI] [PMC free article] [PubMed] [Google Scholar] Motaghinejad M., Fatima S., Karimian M., Ganji S

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