R. J. DeBerardinis

This study shows that pathogenic mtDNA mutations in melanoma cells reduce metastasis by limiting circulation entry, despite promoting tumor growth.

This study shows that lysosomal-mitochondrial interaction (LMI) promotes tumor growth in squamous cell carcinoma of the head and neck by enhancing mitochondrial complex I activity and lysosomal function.

This paper develops an in vitro method using human plasma-like medium to study glioma metabolism and immune interactions, revealing microenvironment-dependent metabolic features and immune responses.

This study shows that ETC inhibition in cancer cells increases reliance on purine salvage and transport, revealing a metabolic vulnerability in tumors with low oxidative metabolism.

This study shows that FASN-deficiency leads to a cytosol-to-mitochondria citrate flux via IDH1 and CTP, which helps cancer cells resist oxidative stress during detachment.

This study investigates mitochondrial metabolism in kidney cancers, finding that primary tumors have suppressed mitochondrial function while metastases show enhanced TCA cycle labeling.

The paper identifies multiple glutamine metabolism pathways in ccRCC tumorgrafts and shows that targeting amidotransferase activity reduces tumor growth.

This study shows adipocytes reprogram cancer cell glucose metabolism to promote metastasis by increasing lipid synthesis via HIF1 regulation.

This study curates genes associated with NE transdifferentiation in SCLC and compares transcriptomic changes across multiple datasets to create a web tool for exploring NE transdifferentiation in SCLC and NBL.

This paper develops an MS method to analyze all 16 aspartate and 32 glutamate isotopomers with high sensitivity, enabling pathway discrimination and metabolic heterogeneity studies in human tumors.

This study shows dimethyl fumarate inhibits serine synthesis and increases glycolysis in endothelial cells, potentially explaining its anti-angiogenic effects.

This study identifies de novo pyrimidine synthesis as a therapeutic target in IDH mutant gliomas, showing that DHODH inhibitors are effective in preclinical models.

This study shows that G6PD deficiency in melanoma cells increases oxidative stress and glutaminolysis, reducing metastasis by making cells more vulnerable to metabolic disruption.

This study identifies a non-canonical glutamine metabolism pathway in DLBCLs where mitochondrial pyruvate supports glutaminolysis and proliferation, particularly in solid extracellular matrix environments.

The paper compares five T cell expansion protocols and finds they induce distinct metabolic programs and phenotypes, with some conditions impairing T cell function despite metabolic adaptation.

This study investigates the tissue-specific roles of mitochondrial complex I and IV in adult mouse liver, finding that complex I loss is tolerated while complex IV dysfunction causes metabolic and functional impairments.

This study examines the relationship between neuroendocrine and immune gene expression in SCLC, finding that variant SCLC tumors regain immune gene expression and exhibit higher tumor-immune interactions.

This study identifies 1-methylnicotinamide (MNA) as an immune regulatory metabolite in high-grade serous ovarian cancer, showing its role in modulating T cell function through non-cell autonomous mechanisms.

The paper identifies the hexosamine biosynthesis pathway as a metabolic vulnerability in KRAS/LKB1 mutant lung cancers and shows GFPT2 inhibition reduces tumor growth.

The paper quantifies metabolic features in NSCLC cell lines to explore associations between metabolism and other cell-autonomous processes.