Targeting Nuclear FGF Receptor to Improve Chemotherapy Response in Triple-Negative Breast Cancer.

摘要

During this funding period, we determined an optimal window of time (8 days post chemotherapy-treatment) in which to study chemo-resistance signaling in chemo-residual triple-negative tumor cells, establishing an in vitro model of triple-negative breast cancer dormancy/recurrence. This work resulted in a manuscript publication. Using this model, we investigated the effect of reducing FGF receptor 2 expression in TN tumor cells on their chemo-resistance. This data showed that FGFR2 does not drive chemoresistance in this breast cancer sub-type, disproving our original hypothesis. Using a Novartis FGFR inhibitor, we confirmed a role for FGFR family members in TN tumor resistance, and obtained new data implicating FGF receptor 3 in this function. These data provide a foundation for testing FGFR3 regulation of TN tumor cell chemo-resistance in the next grant period.