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Use of (18)F-FDG uptake as a surrogate marker of therapeutic response requires the recognition of biologic factors that influence cancer cell glucose metabolism. Estrogen is a potent stimulator of breast cancer proliferation, a process that requires sufficient energy, which is likely met by increased glycolysis. We thus explored the effect of estrogen on (18)F-FDG uptake in responsive breast cancer cells and investigated the mediating molecular mechanisms.

17β-Estradiol Augments 18F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation