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by Paulette Krishack
Post-doctoral fellow in the University of Chicago’s Department of Medicine

Breast cancer is one of the most commonly diagnosed cancers in women. Approximately one in eight will develop the disease in their lifetime, and over 40,000 in the U.S. will die from it this year. While genetics plays a role, 85 percent of women diagnosed with breast cancer have no family history, and effective prevention and treatment depends on identifying the other factors involved.

Clinicians break down breast cancers into at least five types, based on the molecular features present in the tumor cell. Several types are known to show hormone “receptors” (most commonly estrogen, progesterone, and a protein called HER-2) which offer targets for treatment.

But in one type, triple negative breast cancer (TNBC), tumor cells lack the hormone receptors and HER-2 protein known to fuel breast cancer. Finding a way to specifically target TNBC, a particularly aggressive form of cancer, is critical.

Obesity is known as a risk factor for breast cancer incidence and progression. Because obesity can cause chronic, systemic inflammation, Lev Becker, PhD, Marsha Rosner, PhD, and Payal Tiwari, PhD, were interested in finding out how the immune system might be involved in TNBC.

Becker has dedicated his laboratory and career to studying macrophages, the “big eaters” of the immune system, while Rosner specializes in cancer therapeutics. Although macrophages are powerful fighters of viruses and bacteria, they can also be called in to engulf the saturated fatty acids found in many high-fat foods, causing high-fat induced inflammation in the tissues they invade. Becker, Rosner, and Tiwari wanted to see if these obesity-associated macrophages were involved in TNBC.

Using a mouse model of TNBC, they found that the most common macrophages in the breast fat tissue of obese mice were a type specifically activated by a high-fat diet. These macrophages produced a pro-inflammatory protein, a cytokine called IL-6, which created a nurturing environment for TNBC tumors to grow. The team also found that switching the obese mice to a low-fat diet slowed tumor development. Studies also showed human tumor tissue with similar results: there were fewer macrophages present in tissues from lean patients than obese ones.

These studies suggest that immunotherapy—treatments targeting the immune response that is activated by macrophages—may offer innovative care for patients with TNBC, especially if they are obese. They may also offer potential strategies for treating other diseases linked to obesity, particularly those that involve macrophages, such as cardiovascular disease.

Most importantly, this research demonstrates the value of diet in maintaining health. A third of American adults are obese and another third overweight. Now that we know the toll a high-fat diet exerts on molecules in our body, we can embrace the mission of the Duchossois Family Institute: Use the knowledge we develop to improve our health and all those with whom we share the planet.