Zachary T. Schug

TL;DR: A critical role for acetate consumption in the production of lipid biomass within the harsh tumor microenvironment is concluded, indicating a critical role in the growth of cancer cell growth under low-oxygen and lipid-depleted conditions.

TL;DR: It is shown that cardiolipin is required for apoptosis in the type II mitochondria-dependent response to Fas stimulation, and provides an anchor and activating platform for caspase-8 translocation to and embedding in the mitochondrial membrane, steps that are necessary for an efficient type II apoptotic response.

TL;DR: A genetic mouse model is used to reveal a two-pronged mechanism of fructose-induced de novo lipogenesis in the liver, in which fructose catabolism in hepatocytes provides a signal to promote lipogenesis, whereas fructose metabolism by the gut microbiota provides acetate as a substrate to feed lipogenesis.

TL;DR: It is now apparent that CL acts as a crucial signalling platform from which it orchestrates apoptosis by integrating signals from a variety of death inducing proteins.

TL;DR: How acetate functions as a nutritional source for tumours and as a regulator of cancer cell stress is discussed, and how preventing its capture by cancer cells may provide an opportunity for therapeutic intervention.