Clinicians may be able to more accurately predict a woman’s risk of breast cancer, as researchers from the University of Adelaide and the Hospital Research Foundation have identified a gene that contributes to tumor development in women with dense breasts.

The gene—called CC-chemokine ligand 2 (CCL2)—normally attracts immune cells to sites of tissue injury and inflammation. However, overexpression of the gene causes low-level inflammation that contributes to an increased cancer risk through genetic mutations, genomic instability and early tumor promotion. Additionally, constant inflammation can lead to collagen deposition, increasing breast density.

The link between dense breasts and a higher risk for cancer is well established, but the mechanisms that cause dense breasts are less familiar. Study authors wanted to investigate the effects of the gene itself using mouse models. They induced CCL2 overexpression in mammary tissue, finding increased numbers of macrophages to be the root cause of the denser breasts.

“While it is already known that certain types of anti-inflammatories (such as aspirin) can reduce breast cancer risk, they are associated with longer term side effects and not recommended for women to help reduce their breast cancer risk,” said lead author Wendy Ingram, PhD, an associate professor from the University of Adelaide. “With this research we believe we may be able to identify the women most at risk of inflammation-associated breast cancer through measuring their breast density and therefore identify those who will most benefit from anti-inflammatory treatment.”

In fact, the basis for dense breasts may be that inflammatory response, according to study authors. Breast tissue with an overexpression of CCL2 bore a striking resemblance to the clinical presentation of dense breasts, leading the authors to call for additional research.

“Future studies will examine how CCL2 is regulated in the mammary gland, and the biological function of CCL2 in increasing mammographic density in women,” the authors wrote. “Understanding the underlying cellular mechanisms of how inflammation affects breast function will shed light on cancer susceptibility and may uncover new opportunities to therapeutically reduce breast cancer risk.”