Gina M. DeNicola

The paper shows cancer cells in the lung take up cysteine and cystine efficiently, and the reduced tumor microenvironment supports their growth and resistance to oxidative stress.

The paper introduces an anesthesia-free infusion technique for in vivo metabolic tracing in mice, achieving steady-state labeling comparable to jugular infusion without excessive cystine accumulation.

The paper develops microtumor models from lung cancer samples to study EMT and metabolic changes, identifying fatty acid synthesis as a targetable vulnerability.

This study shows mitochondrial copper stabilizes lipoylated TCA cycle proteins, maintaining metabolism and proliferation by supporting lipoylation and TCA cycle function.

This study shows that reduced hepatic phosphatidylcholine biosynthesis leads to copper deficiency, which promotes MASH through disrupted copper distribution and fibrogenesis.

This study identifies QPRT as a non-canonical apoptosis regulator in NSCLC that suppresses caspase-3 activation, independent of its role in NAD biosynthesis, suggesting it as a therapeutic target.

The paper identifies metabolic differences between ASCL1-high and low SCLC cells, showing that ASCL1-high cells resist ferroptosis via BH4/BH2 antioxidants and are vulnerable to combined cysteine depletion and BH4/BH2 inhibition.

This study shows that extracellular glutathione supports tumor growth by providing amino acids through catabolism, and inhibiting this process slows tumor growth.

This study identifies PHGDH as a driver of PDAC progression by maintaining glutamine metabolism and mTOR signaling, revealing a therapeutic vulnerability to glutamine antagonism in PHGDH-deficient tumors.

The paper identifies TXNRD1 as a therapeutic target in KRAS-WT and KRASi-resistant lung cancers by showing TRXR1 inhibition induces ferroptosis through redox mechanisms.

This study uses PET imaging to assess NRF2 activation in NSCLC, showing [18F]FSPG as a marker of therapeutic resistance and a potential target for treatment.

This study identifies PHGDH induction via MAPK and mTORC1 pathways as essential for melanoma formation and shows that combining BRAFV600E inhibition with serine restriction can target this vulnerability.

This paper develops genetic tools for stable circRNA overexpression in vitro and in vivo, demonstrating their utility in cell culture and mouse models.

The paper shows that yeast cells lacking Met15 can assimilate inorganic sulfur via Yll058w, but require exogenous methionine or hydrogen sulfide chelators to grow, challenging the traditional view of MET15 as essential for sulfur assimilation.