Matthew G. Vander Heiden

The paper shows DNA replication stress redistributes G9a to stalled forks, activates gamma-globin genes, and explains how hydroxyurea increases fetal hemoglobin in sickle cell anemia.

This study provides structural insights into DHODH catalysis and drug resistance by analyzing conformational changes and resistance mutations.

This study shows that physiological folate levels limit nucleotide synthesis in leukemia cells, making them reliant on salvage pathways for proliferation.

This paper shows that asparagine enables transsulfuration to restore redox balance in tumors lacking aspartate synthesis enzymes, highlighting transsulfuration as a targetable vulnerability.

This study shows that α-ketoacids enhance the effectiveness of bortezomib by reducing cysteine-mediated detoxification, thereby increasing proteasome inhibition and cytotoxicity.

The paper identifies a metabolic vulnerability in TP53-deficient cells linked to nuclear adenosine metabolism and histone methylation, showing its role in DNA damage response and tumor growth.

This study shows pancreatic cancer disrupts normal pancreatic function, leading to systemic nutrient depletion and muscle wasting, with autophagy in muscle playing a key role in nutrient redistribution to support tumor growth.

This study uses intraoperative arteriovenous sampling to measure tumor metabolism in NSCLC patients, revealing distinct metabolic profiles between tumor and normal lung tissue.

The paper investigates how amino acid limitation affects translation by analyzing ribosome stalling and the role of RQC pathways and RNF14 in response to arginine depletion.

This study shows that single nutrients do not determine breast cancer metastasis sites, and identifies purine synthesis as a key factor across multiple tissues.

This study shows that acetoacetate suppresses colon cancer by expanding and activating MAIT cells via the MR1 receptor, offering a potential immunotherapy approach.

This study shows that dietary cysteine improves intestinal stem cell repair through IL-22 from CD8+ T cells.

This study compares nutrient levels in plasma and bone marrow of pediatric B-ALL patients, identifying metabolic differences between subtypes and highlighting unique metabolic features in B-ALL circulation.

This study shows that inhibiting formate production in CD8+ T cells delays type 1 diabetes onset in mice by reducing their activation and effector function.

This study identifies riboflavin as a critical metabolic dependency in acute myeloid leukemia, showing its role in nucleotide biosynthesis and iron-sulfur cluster metabolism beyond energy production.

The paper identifies sideroflexins as mitochondrial transporters for neutral amino acids and shows functional overlap among paralogues.

This study shows that loss of UFMylation promotes prostate cancer metastasis by reprogramming glucose metabolism towards hexosamine biosynthesis.

The paper shows cancer cells adjust mitochondrial respiration to alter NAD+/NADH ratios, enhancing biomass synthesis and proliferation under nutrient limitation.

This study examines how aging affects glucose and lipid metabolism in mice, finding that NAD+ levels remain stable but lipid metabolism increases in aged tissues.

The paper identifies off-target activation of GCN2 by BRAF and EGFR inhibitors, showing it limits cancer cell proliferation.

This study identifies sex-specific metabolic reprogramming in obesity by analyzing phosphorylation sites on metabolic enzymes and their functional impact.

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

The paper shows genomic uracil induces DNA replication stress without BER processing and identifies UNG2 upregulation as a vulnerability in cancer cells.

The paper quantifies the relationship between compartmentalized NADPH dynamics and cancer cell growth rates using a composite index analysis and identifies key transporters involved in this relationship.

This study profiles metabolites in renal cell carcinoma tissue and fluid to show that nutrient availability is more influenced by tissue-specific factors than tumor-driven changes.

The paper identifies PRDX1 as essential for DNA damage repair by scavenging nuclear ROS and regulating aspartate synthesis during the DNA damage response.

This study shows Yap regulates glucose utilization and nucleotide synthesis to support organ growth in zebrafish, with conserved mechanisms in mammals.

This study shows that increased PHGDH expression in mice leads to premature melanin accumulation in hair follicles, suggesting a role for PHGDH in melanocyte biology and potential involvement in melanoma.