Philip L. Lorenzi

The paper benchmarks nDIA and related proteomics methods, showing nDIA with DIA-NN and Tesorai Search provides high coverage and reliable results in proteomic analysis.

The paper identifies biallelic KMO variants as a novel cause of congenital NAD deficiency and shows gene x environment interactions in a mouse model.

This study shows that colorectal cancer in mice and rhesus macaques causes inflammatory neuropathy with calcium dysregulation and myelin issues, suggesting a causal link to chronic neurological problems in cancer survivors.

This study shows aerobic exercise improves PDAC vascular function and chemotherapy efficacy via S1PR1 signaling in tumor endothelial cells.

This study shows KDM6A mutations in bladder cancer improve response to immune checkpoint therapy but worsen chemotherapy outcomes through effects on DNA repair and metabolic reprogramming.

This study shows that reduced hepatic pyrimidine synthesis during fasting and obesity promotes insulin resistance and obesity by increasing hepatic glucose production and decreasing insulin clearance.

The paper identifies ASX-173 as a potent ASNS inhibitor that enhances the anti-cancer effects of L-asparaginase in leukemia and shows its potential across multiple cancer types.

This study shows that loss of LATS1/2 in endothelial cells promotes a senescence-associated stemness (SAS) state, leading to atherothrombotic plaque formation through metabolic and mitochondrial dysregulation.

This study identifies mitochondrial dysfunction and metabolic reprogramming in MSH2-deficient endometrial cancer, revealing a novel pathway and potential therapeutic targets.

The paper uses multi-omic mass spectrometry to analyze drug toxicity mechanisms in mice, identifying pathways involved in ASNase toxicity and proposing potential mitigation strategies.

This study shows that disrupting the WRAD core in pancreatic cancer leads to DNA replication errors, immune response activation, and improved response to immune checkpoint inhibitors.

The paper introduces UFP-MS, a fast proteomics method, and applies it to study drug effects on mouse tissues, revealing tissue-specific metabolic changes.

This study identifies ROCK inhibition as a strategy to overcome metabolic adaptation in cancer cells to OXPHOS inhibition, showing synergistic anti-tumor effects.

This study shows that ACL loss in the heart increases glucose oxidation and reduces citrate efflux, leading to metabolic remodeling and cardiac dysfunction.

TARO integrates microbiome and metabolomic data to identify cross-platform associations by leveraging phylogenetic tree structures and structured sparsity.

This study shows that D2-HG induces cachexia in mice by disrupting NAD+ homeostasis and autophagy, revealing metabolic vulnerabilities in skeletal muscle.