A recent study has purportedly found that “high levels of glucose in the diet of mice with cancer is linked to increased expression of mutant p53 genes,” raising questions about the effect of a high-sugar diet on tumor growth. Olga Catalina Rodriguez, et al., “Dietary downregulation of mutant p53 levels via glucose restriction: Mechanisms and implications for tumor therapy,” Cell Cycle, November 2012.

According to a concurrent Georgetown University Medical Center (GUMC) press release, normal p53 acts as a tumor suppressor but mutant p53 acts as an oncogene, with high levels of expression “linked to cancer aggressiveness, resistance to therapy, worse outcomes and even relapse after therapy.”

The five-year study apparently examined how glucose restriction (GR) affected autophagy—the degradation of dysfunctional proteins—in cultured cells and tumor growth in animal models. The first experiments not only suggested that GR helped eliminate p53 mutant proteins via autophagy, but that transgenic mice fed a low-glucose diet showed “a significant decrease in the amount of mutant p53 protein in their tissues, compared to mice fed with a high carbohydrate diet.” A second set of experiments allegedly determined that in mice engineered with human lung cancer cells, a low-carbohydrate diet effectively blocked tumor growth, “but only when the tumors expressed the mutant p53 protein that could be degraded by autophagy.”

“This series of studies helps establish the mechanisms of why a low carbohydrate diet slows tumor growth. Glucose restriction triggers autophagy, a critical process for clearing the cell of detrimental, potentially damaging proteins or cellular debris that can eventually destroy the entire cancer cell. We believe that this process works more efficiently when mutant p53 is not around,” the lead author was quoted as saying. “Various types of dietetic interventions have been shown to affect cancer growth, but no one had ever shown, before this study, that the amount of carbohydrates could affect the expression of mutant p53.”