C. A. Lyssiotis

This study shows that sulfide oxidation via SQOR promotes hypoxic angiogenesis and neovascularization by reprogramming metabolic pathways in endothelial cells.

This paper shows type I interferon coordinates immunometabolic checkpoints during Staphylococcal infection by regulating metabolic and inflammatory programs in macrophages.

This study shows that G6PD deficiency accelerates pancreatic acinar-to-ductal metaplasia by enhancing NADPH production for ROS management, highlighting a metabolic role in early tumorigenesis.

This study shows that H2S preconditioning causes long-lasting changes in O2 metabolism, including increased P50(O2) and metabolic memory effects lasting up to 24-48 hours.

This study identifies tissue- and subset-specific roles of SLC38A1 in Th1 cell function during inflammation, showing its importance in EAE and IBD but not lung inflammation.

This study identifies de novo purine metabolism as a vulnerability in cancers with low p16 expression, showing sensitivity to anti-folate drugs like methotrexate.

This study identifies a GTP-mediated signaling pathway linking metabolism to DNA repair and resistance to genotoxic stress in glioblastoma and non-malignant cells.

The paper shows that fever increases inflammatory activity in CD4+ T cells but causes mitochondrial dysfunction and DNA damage specifically in Th1 cells, leading to p53-dependent apoptosis to prevent mutations.

This study shows PINK1 supports colorectal cancer growth by regulating the labile iron pool through mitophagy and ferritinophagy.

The paper shows cardiolipin regulates Complex II assembly and stability in macrophages, linking it to inflammatory metabolic reprogramming.

This study shows that Arginase 1 suppresses immune responses in pancreatic cancer by inhibiting T cell activation, and targeting it enhances immunotherapy effectiveness.

This study shows that ammonia accumulation in the colorectal cancer microenvironment promotes T cell exhaustion and treatment resistance, and that reducing ammonia improves immunotherapy efficacy.

This study shows that high glucose levels increase the effectiveness of chemotherapy in pancreatic cancer by reducing glutathione biosynthesis, which enhances oxidative stress in cancer cells.

This study identifies metabolic vulnerabilities in DIPG subtypes and shows that targeting these vulnerabilities with specific drugs can extend survival in preclinical models.

This study identifies NetrinG1+ cancer-associated fibroblasts that produce extracellular vesicles supporting pancreatic cancer cell survival under nutrient stress.

This study shows that OXPHOS enhances TH17 cell survival and persistence by promoting mitochondrial fitness and anti-apoptotic markers.

This study identifies metabolic markers and pathways in pancreatic tumor-associated macrophages using multi-omic analysis and in vitro models.

The paper identifies a redox cycle involving complex II and SQOR that sustains H2S oxidation when complex IV is inhibited, improving H2S clearance in cells exposed to microbiota-derived H2S.

This study shows that extrinsic KRAS signaling reprograms pancreatic fibroblasts to create an inflammatory microenvironment that supports tumor growth.

This study shows that overexpressing SIRT5 protects against cardiac dysfunction and fibrosis in response to pressure overload in mice.

This study identifies uridine as a novel nutrient for pancreatic cancer cells through uridine phosphorylase 1, showing its role in survival and metabolism under glucose deprivation.

The paper identifies consistently expressed genes in pancreatic ductal adenocarcinoma (PDAC) to prioritize therapeutic targets and biomarkers.

This study shows human norovirus infects primary B cells, induces functional changes, and the NS1 protein affects B cell proliferation and metabolism in vitro.

This study identifies reuterin as a microbial metabolite that suppresses colorectal cancer growth by altering redox balance and inducing cell death.

This study identifies MCAD as a critical enzyme for fatty acid metabolism in GBM, showing its essential role in preventing mitochondrial damage and apoptosis.

This study shows hyaluronic acid fuels pancreatic cancer metabolism by bypassing GFAT1 via the GlcNAc salvage pathway, enabling proliferation in nutrient-starved conditions.

This study identifies SIRT5 as essential for melanoma cell survival and tumor formation, showing it regulates chromatin dynamics and gene expression through histone modifications.

This study shows that the pancreatic tumor microenvironment compensates for loss of GOT2 by providing pyruvate, maintaining redox homeostasis and tumor growth in vivo.

The paper identifies two metabolic subclasses in pancreatic cancer cells and shows asparagine's role in supporting proliferation under mitochondrial stress, suggesting a new therapeutic strategy.