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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.
This idea proposes mapping metabolic dependencies in the patient rather than the dish: tumours switch fuels, so measuring what a tumour consumes with PET tracers could match drug to tumour. Isotope tracing in patients (DeBerardinis) shows in vivo fuel use differs from culture, FDG, glutamine (18F-FGln) and acetate tracers exist, and glutaminase inhibitors failed in unselected populations. The hypothesis is that tracer-defined phenotypes (glycolytic, glutamine- or lipid-dependent) predict response to matched inhibitors, because imaging reads tumour metabolism non-invasively. The test is a basket trial assigning therapy by baseline 18F-FGln and FDG PET in Non-small-cell lung cancer, Renal cell carcinoma and Glioma & glioblastoma (Cancer metabolism pathway).
Shares MD Anderson Cancer Center, Memorial Sloan Kettering Cancer Center, Glioma & glioblastoma and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center, Non-small-cell lung cancer and the tags mechanism, open-question.
Shares MD Anderson Cancer Center, Non-small-cell lung cancer and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center and the tags mechanism, open-question.
Shares Memorial Sloan Kettering Cancer Center and the tags mechanism, open-question.