Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth.

The Dietary Supplement Chondroitin-4-Sulfate Exhibits Oncogene-Specific Pro-tumor Effects on BRAF V600E Melanoma Cells. Mutant and Wild-Type Isocitrate Dehydrogenase 1 Share Enhancing Mechanisms Involving Distinct Tyrosine Kinase Cascades in Cancer. ?-6-Phosphogluconolactone, a Byproduct of the Oxidative Pentose Phosphate Pathway, Contributes to AMPK Activation through Inhibition of PP2A. Lysine acetylation restricts mutant IDH2 activity to optimize transformation in AML cells. Lyso-PAF, a biologically inactive phospholipid, contributes to RAF1 activation.

University of Science and Technology of China Two major research focuses include (1) To determine both metabolic and signaling functions of intracellular metabolites and circulating “blood chemicals”, which influence tumorigenesis and tumor progression, and responses to anti-cancer therapies including chemotherapy and immunotherapy and (2) To decipher mechanistic basis underlying the pathogenic links between diets and particular oncogenic mutations by exploring the pro- and anti-tumor effects of diet-derived substances on tumors with specific genetic backgrounds. Chen is interested in elucidating the signaling interplay between metabolic and cell signaling networks for a better understanding of cancer metabolism and improved clinical outcome.

Jing chen university of georgia