The Lyons laboratory focuses on mechanisms of lymphatic mediated metastasis of breast cancer. Specifically, we utilize mouse models of breast cancer to investigate developmentally regulated programs of inflammation and lymphangiogenesis that are utilized in the adult mammary gland and may be hijacked by breast tumor cells. The results of these translational studies have the potential to instruct therapy aimed at prevention of breast cancer metastasis.

In the past decade, postpartum breast cancers have emerged as a highly metastatic subset of young women’s breast cancer(1, 2). While definitions of postpartum breast cancer vary, increased metastasis and decreased survival is consistently observed in women who are diagnosed with breast cancer after pregnancy(3-6). Our recently published studies indicate that women diagnosed with breast cancer within 2-3 years postpartum have increased incidence of lymph node metastasis and increased lymphatic vessel density in the tumor microenvironment. Further, in animal models we have shown that pro-inflammatory enzyme cyclooxygenase-2 is a driver of metastasis as well as lymphangiogenesis in the tumor microenvironment(7, 8). Importantly, specific inhibitors of COX-2 block lymphangiogenesis in both normal mammary tissue and in the tumor microenvironment, suggesting that anti-COX-2 therapies may inhibit metastasis by blocking lymphangiogenesis(8).

Current studies in the Lyons lab focus on the mechanisms that cells of the normal mammary tissue, postpartum tumor cells, as well as breast cancer cells in general, utilize to increase the number of lymphatic vessels. In addition, we also wish to determine whether the process of tumor cell recruitment and invasion of lymphatic structures is dependent on COX-2 and other known pro-lymphangiogenic factors. The ultimate goal of our work is to identify targets for therapeutic intervention and chemoprevention in young women at risk for breast cancer and breast cancer metastasis and to advance these targets to clinical trail.