show Abstracthide AbstractNintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes Overall design: In order to gain insight into the mechanisms underlying Nintedanib and Alpelisib synergism in vivo, we tested the effects of Nintedanib, Alpelisib (BYL719) and their combination on Nintedanib-resistant VM-CUB-1 cells xenografts. We performed RNA sequencing of tumors treated for 7 days with either either vehicle (n=4), Nintedanib [responders (n=2) and non-responders (n=3)], Alpelisib (n=4), or their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes