ideasIdea
Map metabolic dependencies in the patient, not the dish
Metabolic drugs keep failing because tumours switch fuels. Measuring what a patient's tumour actually eats, with tracers and PET, could pick the right metabolic drug for the right tumour.
Isotope tracing in patients (DeBerardinis) shows in vivo fuel use differs from culture; FDG, glutamine (18F-FGln), and acetate PET tracers exist; glutaminase and other agents failed in unselected populations.
Hypothesis
Tracer-defined metabolic phenotypes (glycolytic, glutamine-dependent, lipid-dependent) predict response to matched metabolic inhibitors, rescuing agents that failed in unselected trials.
Rationale
Tumour metabolism is heterogeneous and plastic; imaging can read it non-invasively and repeatedly.
What would test it
Basket trial with baseline 18F-FGln and FDG PET assigning glutaminase inhibitor or glycolysis-targeting agent, with PET flux change at 2 weeks as pharmacodynamic endpoint.
Maturity
preclinical evidence