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 sucroseenriched 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 sugarpromoted tumor growth in mice. How dietary sucrose and fructose induces 12-HETE and whether it has a direct or indirect effect remains in question.”