Abstract #3896

Response to glutaminase inhibition in patient-derived breast cancer xenograft models

Maria Tunset Grinde¹, Jana Kim¹, Ida Marie Henriksen¹, Hanna Maja Tunset¹, and Siver Andreas Moestue^2,3

¹Dept. of Circulation and Medical Imaging, NTNU (Norwegian University of Science and Technology), Trondheim, Norway, ²Dept. of Clinical and Molecular Medicine, NTNU (Norwegian University of Science and Technology), Trondheim, Norway, ³Dept. of Pharmacy, Nord University, Bodø, Norway

We used ex vivo 13C HR MAS MRS to determine glutamine consumption and conversion in two patient-derived xenograft models of breast cancer, aiming to identify metabolic differences between a responding (luminal-like) xenograft and a resistant (basal-like) xenograft. CB-839 inhibited tumor growth in luminal-like, but not basal-like, xenograft tumors. Response to treatment was associated with differences in glutamine utilization. Depletion of proline in responding tumors indicate that the effect of glutaminase inhibitors may be associated with metabolic adaption to tumor hypoxia.

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