G. M. DeNicola

The paper screens drugs in human physiologic medium and identifies uric acid as an inhibitor of rigosertib's efficacy.

This study shows that glutathione (GSH) is essential for lipid abundance in adult tissues, particularly in the liver, by repressing NRF2.

The paper shows that mitochondrial function is preserved under cysteine starvation via glutathione catabolism in NSCLC cells, preventing ferroptosis.

This study investigates cysteine metabolism in normal and tumor tissues using isotopic tracing, finding that cystine uptake is universal while de novo synthesis and catabolism vary across tissues and tumor types.

This study investigates the role of Nrf2 signaling thresholds in lung tumor initiation and progression using murine models with KEAP1 and NRF2 mutations.

This study identifies NADK upregulation as a critical metabolic adaptation enabling breast cancer metastasis by enhancing NADPH production and oxidative stress resistance.

This study uses a CRISPR screen to identify redox vulnerabilities in KEAP1/NRF2 mutant NSCLC, finding that SOD2 loss enhances the efficacy of β-Lapachone by disrupting mitochondrial function.

This study shows that fascin promotes lung cancer growth and metastasis by enhancing glycolysis through YAP1-PFKFB3 activation.

This study establishes a living biobank of patient-derived organoids from intraductal papillary mucinous neoplasms to study their progression and identify biomarkers for early detection and prevention.

This study identifies a non-canonical role of glutamate-cysteine ligase in preventing glutamate accumulation and ferroptosis under cystine starvation.

This study shows that NRF2/KEAP1 mutations confer resistance to β-lapachone by enhancing ROS detoxification, and that inhibiting SOD1 or the thioredoxin system can overcome this resistance.

This study shows PHGDH depletion in adult mice is tolerated, with normal liver and pancreatic function, but reduced PHGDH leads to altered lipid homeostasis in the liver.

This study shows NNT promotes NSCLC tumor growth by maintaining Fe-S protein function through NADPH production, preventing mitochondrial dysfunction and ROS accumulation.

The paper identifies CDO1 as a metabolic liability in NSCLC by showing its silencing promotes proliferation through cysteine metabolism disruption.