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Postpartum Breast Cancer

Department of Medicine


A mouse model of postpartum breast cancer that identifies mammary gland involution as a driving force of tumor progression

Tumor cells (T) on collagen rich stroma (S) upregulate COX-2Faculty and Post-Docs within the Department of Medicine regularly study and publish groundbreaking research. We are excited to highlight published research papers.

This paper's research on postpartum breast cancer was conducted primarily by Postdoctoral Fellow in the Department of Medicine Division of Medical Oncology, Traci R. Lyons, PhD, and Postdoctoral Fellow in the School of Pharmacology, Jenean H. O'Brien, PhD, along with other colleagues.

Postpartum mammary gland involution drives progression of ductal carcinoma in situ through collagen and COX-2. Nature Medicine 2011, 17: 1109-1115.

Abstract: Reproductive history influences the prognosis of breast cancer in young women. Women diagnosed within 5 years postpartum have worse prognosis than nulliparous women or women diagnosed during pregnancy. In this research paper the authors describe a mouse model of postpartum breast cancer that identifies mammary gland involution as a driving force of tumor progression. In this model, human breast cancer cells exposed to the involuting mammary microenvironment form large tumors that are characterized by abundant fibrillar collagen, high cyclooxygenase-2 (COX-2) expression and an invasive phenotype. In culture, tumor cells are invasive in a fibrillar collagen and COX-2–dependent manner. In the involuting mammary gland, inhibition of COX-2 reduces the collagen fibrillogenesis associated with involution, as well as tumor growth and tumor cell infiltration to the lung. These data support further research to determine whether women at high risk for postpartum breast cancer would benefit from treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) during postpartum involution.​