Metabolism and Cancer
The energetic demands of cancer cells have been described as the “sweet tooth” of cancer. The metabolic adaptations of cancer cells were realized over 80 years ago, but recent studies revealed important interactions with metabolism of the host tissues.
The Yadava laboratory has shown that modest declines in mitochondrial function, equivalent to the loss that occurs by age 70 in humans, profoundly interferes with the activity of the p53 tumor suppressor pathway and inflammatory responses. Analyses of primary breast epithelial cells are revealing the extent of the variation in metabolic sufficiency among patients and the consequences on tumor suppressor pathways (Schneider, Yadava).
Rapid uptake of glucose and lactate, and not hypoxia, induces apoptosis in three-dimensional tumor tissue culture (Forbes) providing novel targets and mechanisms. Obesity and type 2 diabetes also alter the host environment through increased inflammatory pathways and growth factors favoring promotion of tumors (Liu, Makari-Judson, Schneider, Schneyer). The Energy Metabolism Laboratory (Freedson) provides expertise in designing interventions targeting metabolism in human subjects.
Together these researchers offer skills extending from cellular respiration in cell-based assays to whole-body metabolic measures in human subjects.