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

Breast cancer resistant to either doxorubicin or epirubicin relies on distinct primary metabolic processes, which can be targeted to reduce cancer progression.

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.

Isotope tracing into macromolecules enables functional analysis of metabolism in specific cell populations in tumors and provides insight into metabolic differences between cancer and stromal cells in their endogenous microenvironment.

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

The nutrients available in some tumors and the factors that influence tumor nutrient availability are characterized, which provides insight into the metabolic constraints of the tumor microenvironment.

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.

The tumor suppressor APC regulates a metabolic program that drives normal intestinal differentiation in zebrafish.