A new study, published in the journal of Cancer Research by the University of Texas MD Anderson Cancer Center, has specified that the Western diet with its high amount of sugar increase the risk of breast cancer and metastasis to the lungs. The per capita consumption of sugar in the U.S. has substantially increases to over 100 lbs. per year and an increase in consumption of sugar-sweetened beverages has been identified as a significant contributor to an epidemic of obesity, heart disease and cancer worldwide.
“We found that sucrose intake in mice comparable to levels of Western diets led to increased tumor growth and metastasis, when compared to a non-sugar starch diet,” said Peiying Yang, Ph.D., assistant professor of Palliative, Rehabilitation, and Integrative Medicine. “This was due, in part, to increased expression of 12-LOX and a related fatty acid called 12-HETE.”
12-Lox, (12-lipoxygenase), is an enzymatic signaling pathway activated by sugar. The study demonstrates that dietary sugar induces 12-LOX signaling to increase risks for breast cancer development and metastasis. The researchers conducted four different studies where mice were randomized to different diet groups and fed one of four diets. At six months of age, 30 percent of mice on a starch-control diet had measurable tumors, whereas 50 to 58 percent of the mice on sucrose-enriched diets had developed mammary tumors. The study also showed that numbers of lung metastases were significantly higher in mice on a sucrose- or a fructose-enriched diet, versus mice on a starch-control diet.
“The current study investigated the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with mechanisms that may be involved,” said co-author Lorenzo Cohen, Ph.D., professor of Palliative, Rehabilitation, and Integrative Medicine. “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.”
“Prior research has examined the role of sugar, especially glucose, and energy-based metabolic pathways in cancer development,” said Yang. “However, the inflammatory cascade may be an alternative route of studying sugar-driven carcinogenesis that warrants further study.”
“This study suggests that dietary sucrose or fructose induced 12-LOX and 12-HETE production in breast tumor cells in vivo,” said Cohen. “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.”
Yan Jiang, Yong Pan, Patrea R. Rhea, Lin Tan, Mihai Gagea, Lorenzo Cohen, Susan M. Fischer, and Peiying Yang. A Sucrose-Enriched Diet Promotes Tumorigenesis in Mammary Gland in Part through the 12-Lipoxygenase Pathway. Cancer Res, January 1, 2016 76:24-29 DOI: 10.1158/0008-5472.CAN-14-3432