M. G. Vander Heiden

The paper shows that nucleotide depletion and DNA replication stress drive cell fate transitions in hematopoietic systems by activating lineage-specific maturation genes.

The paper shows that removing tumor-draining lymph nodes does not impair immune checkpoint blockade response, as distant lymph nodes compensate for the loss.

The paper screens compounds targeting metabolism in serum-derived medium to identify differential responses in cancer cells, aiming to improve drug response prediction.

This study uses a CRISPRi/a screening platform to identify nutrient transporters critical for cancer cell proliferation in diverse microenvironments and reveals their functional roles.

This study shows that cancer tissue-of-origin influences the metabolism and growth preferences of both primary and metastatic tumors.

This study shows that ablative radiotherapy improves survival in autochthonous cancer mouse models and synergizes with androgen deprivation in prostate cancer.

This study identifies leukemia-intrinsic resistance mechanisms to CAR-T therapy through in vivo CRISPR screening in a murine B-ALL model, revealing IFNγ/JAK/STAT and antigen processing pathways as key mediators.

The paper shows that nucleotide imbalances during S phase disrupt DNA replication and cell proliferation, requiring replication stress signaling for survival.

The paper develops the MIDAS platform to identify protein-metabolite interactions, revealing novel regulatory mechanisms in carbohydrate metabolism.

This study identifies SHMT1 and SHMT2 as therapeutic targets in T-ALL by showing their inhibition impairs leukemia progression and is effective despite methotrexate resistance.

The paper investigates the role of pyruvate kinase isoforms in prostate cancer, finding that Pkm1 suppresses cancer while Pkm2 promotes it, and that a PKM1-like activator can suppress tumor progression.

The paper investigates how interactions with pancreatic stromal cells affect the redox state of cancer cells, finding that these interactions promote a more oxidized redox state in cancer cells.

The paper measures nutrient uptake in the tumor microenvironment using PET tracers and finds cancer cells prefer glutamine while myeloid cells consume most glucose.

This study shows methionine synthase is essential for cancer cell proliferation under physiological folate conditions but not in standard cell culture.

The paper shows that increased NAD+ demand relative to ATP demand drives aerobic glycolysis by impairing NAD+ regeneration and promoting fermentation.

This study identifies Netrin G1 as a promoter of pancreatic ductal adenocarcinoma tumorigenesis by enhancing cancer-associated fibroblast-driven metabolic support and immunosuppression.

This study shows that brain metastases rely on PHGDH-mediated serine synthesis due to limited environmental serine, making them sensitive to PHGDH inhibition.

This study shows that pancreatic stellate cells secrete deoxycytidine, which reduces the effectiveness of gemcitabine in PDAC by inhibiting its processing in cancer cells.

The paper quantifies microenvironmental metabolites in murine cancer models and identifies factors affecting tumor nutrient availability.

The paper shows that environmental cystine levels influence glutamine anaplerosis and glutaminase dependence in cancer cells.