Mammary Gland Tumors Allegedly Linked to Sucrose Consumption
An animal study examining the purported link between high sucrose intake and the development of mammary gland tumors has attributed the effect in part “to increased expression of 12-lipoxygenase (12-LOX) and its arachidonate metabolite 12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE).” Yan Jiang, et al., “A Sucrose-Enriched Diet Promotes Tumorigenesis in Mammary Gland in Part through the 12-Lipoxygenase Pathway,” Cancer Research, January 2016.
University of Texas MD Anderson Cancer Center researchers used several mouse models–“including a mouse mammary gland tumor model that carries a MMTV/unactivated neu transgene, a human triple-negative breast cancer cell (MDA-MB-231) orthotopic mouse model, and a breast cancer lung metastasis mouse model (injected with 4T1 mouse breast cancer cells)”–to identify a potential mechanism by which a sucrose-enriched diet contributes to tumor genesis and metastasis. The study reports that 50 to 58 percent of mice on a sucrose-enriched diet developed mammary tumors, compared to 30 percent on a starch-control diet. It also suggests that those mice fed a diet high in sucrose and fructose showed a significantly higher numbers of lung metastases.
“We determined that it was specifically fructose, in table sugar and high-fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung metastasis and 12-HETE production in breast tumors,” explained one of the authors in a December 31, 2015, press release. “This study suggests that dietary sucrose or fructose induced 12-LOX and 12-HETE production in breast tumor cells in vivo. This indicates a possible signaling pathway responsible for sugar-promoted tumor growth in mice. How dietary sucrose and fructose induces 12-HETE and whether it has a direct or indirect effect remains in question.”
Issue 589
