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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