Oliver D. K. Maddocks

TL;DR: It is shown that human cancer cells rapidly use exogenous serine and that serine deprivation triggered activation of the serine synthesis pathway and rapidly suppressed aerobic glycolysis, resulting in an increased flux to the tricarboxylic acid cycle.

TL;DR: It is shown that serine can bind to and activate human PKM2, and thatPKM2 activity in cells is reduced in response to serine deprivation, which shifts cells to a fuel-efficient mode in which more pyruvate is diverted to the mitochondria and more glucose-derived carbon is channelled into serine biosynthesis to support cell proliferation.

TL;DR: Key issues in interpreting (13)C metabolite labeling patterns are reviewed, with the goal of drawing accurate conclusions from steady state and dynamic stable isotopic tracer experiments.

TL;DR: It is concluded that nucleotide synthesis and cancer cell proliferation are supported by serine--rather than glycine--consumption, and therefore exogenous glycine cannot replace serine to supportcancer cell proliferation.

TL;DR: A better understanding of the metabolic functions of p53 family members may aid in the identification of therapeutic targets and reveal novel uses for p53-modulating drugs.