Targeting the fatty acid oxidation in combination with chemotherapy induces complete pancreatic cancer regression in vivo

Targeting the fatty acid oxidation in combination with chemotherapy induces complete pancreatic cancer regression in vivo

Targeting the fatty acid oxidation in combination with chemotherapy induces complete pancreatic cancer regression in vivo 1125 1625 Metabolism & Cancer
3 Comments
  • Hi Gabriela, thanks for your poster. I’d like to know if you have evaluated ROS levels in your system. Another question regards the experiment in Fig. 1, did you count live cells after treatment with inhibitors? Thank you

    • Thank you Serena for your interesting questions. For the first one, we are currently evaluating ROS levels. In fact, high responder cells to FAO targeting, seem to have higher basal ROS levels. Moreover, Perhexiline treatment is a ROS inductor (dose-dependent), and could increase ROS levels combined with Gemcitabine. For the second question, the assay was done injecting low concentrations of the inhibitors directly during OCR measurements, We didn’t evaluate cell viability after the assay, but in cell viability assays we demonstrate that Etomoxir at the used dose (4 microM) has no impact on cell viability in any of the cells. Good day.