Differential luminal breast cancer (LBC) reprogramming in response to BIBF1120 (BIBF) or bevacizumab (B).

11033 Background: FVB MMTV PyMT is a great mouse model for studying LBC due to its stochastic nature, immune system preservation, natural growth kinetics and ER/HER2 status. We approached the transcriptomic (T), proteomic (P), phospho-proteomic (P-P) and metabonomic (M) layers of regulation of the tumor phenotype attempting to unravel mechanisms of resistance to antiangiogenic drugs (ADs) and find new targets. Methods: Treatments started when tumors measured 0,1cm3; with the VEGFR/PDGFR inhibitor BIBF 85mg/kg/day; a murine analog of B 10mg/kg/biweekly; or vehicle (V). Tumors were harvested at time 0, week 1 (T1), or at sacrifice (Tend, 1cm3). Cd31 and pimomidazole measured vascularization and O2. T; P/P-P; and M layers were interrogated with sure print 3G arrays; titanium separation - HPLC fractionation - orbitrap spectrometer run; and GC/MS and LC/MS. Gene ontology pathways were discovered with GSEAS; kinase networks by consensus domain analysis; metabolic pathways rearrangement with in-house built bioin...