Engineered diets to improve cancer outcomes.

Cancer cells acquire a diverse range of metabolic adaptations that support their enhanced rates of growth and proliferation. While these adaptations help tune metabolism to support higher anabolic output and bolster antioxidant defenses, they can also decrease metabolic flexibility and increase dependence on nutrient uptake versus de novo synthesis. Diet is the major source of nutrients that ultimately support tumor growth, yet the potential impact of diet is currently underutilized during the treatment of cancer.

Control of TSC2-Rheb signaling axis by arginine regulates mTORC1 activity.

The mammalian target of rapamycin complex 1 (mTORC1) is the key signaling hub that regulates cellular protein homeostasis, growth, and proliferation in health and disease. As a prerequisite for activation of mTORC1 by hormones and mitogens, there first has to be an available pool of intracellular amino acids. Arginine, an amino acid essential during mammalian embryogenesis and early development is one of the key activators of mTORC1.

iRFP is a sensitive marker for cell number and tumor growth in high-throughput systems.

GFP and luciferase are used extensively as markers both in vitro and in vivo although both have limitations. The utility of GFP fluorescence is restricted by high background signal and poor tissue penetrance. Luciferase throughput is limited in vitro by the requirement for cell lysis, while in vivo, luciferase readout is complicated by the need for substrate injection and the dependence on endogenous ATP.