Genome-scale metabolic modeling of individual cancer cells and healthy human cells identifies specific and selective metabolic vulnerabilities.

Exosomes from cancer-associated fibroblasts enhance the "Warburg effect" in tumors and contain de novo metabolites that can contribute to the entire compendia of central carbon metabolism within cancer cells.

Activation of the NRF2 antioxidant program leads to an imbalance in central carbon metabolism and sensitizes cancers to glutaminase inhibition.

Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.

Exploiting the metabolic consequences of Akt activation in prostate cancer for therapeutic interventions that circumvent Akt inhibition therapy.

Cell culture models widely used in cancer research do not reflect metabolism in tumors; by altering culture systems to better model tumor metabolism we find that environmental cystine promotes tumor glutamine metabolism.

Mannose phosphate isomerase is a metabolic enzyme regulating cell survival in both embryonic and cancer cells.

By increasing intracellular cysteine levels, NRF2 engages a tumor suppressive metabolic pathway mediated by cysteine dioxygenase 1.

Many tumors are depleted of mitochondrial DNA; this depletion is associated with changes in gene expression and with the incidence of critical somatic mutations and alterations.