Kevin Marks

TL;DR: It is shown that cancer-associated IDH1 mutations result in a new ability of the enzyme to catalyse the NADPH-dependent reduction of α-ketoglutarate to R(-)-2-hydroxyglutarate (2HG), and that the excess 2HG which accumulates in vivo contributes to the formation and malignant progression of gliomas.

TL;DR: Results reveal that certain breast cancers are dependent upon increased serine pathway flux caused by PHGDH overexpression and demonstrate the utility of in vivo negative-selection RNAi screens for finding potential anticancer targets.

TL;DR: The metabolic enzyme, methionine adenosyltransferase II alpha (MAT2A), and the arginine methyltransferase, PRMT5, are identified as vulnerable enzymes in cells with MTAP deletion, creating an axis of targets vulnerable in CDKN2A/MTAP-deleted cancers.

TL;DR: Induction of serine auxotrophy by PKM2 activation was accompanied by reduced carbon flow into the serine biosynthetic pathway and increased expression of high affinity serine transporters, supporting the hypothesis that PKM1 expression confers metabolic flexibility to cancer cells that allows adaptation to nutrient stress.

TL;DR: High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetically lethal with LKB1 deficiency in mouse and human lung cancer lines, suggesting that DTYMK is a potential therapeutic target in this aggressive subset of tumors.