115īreast cancers diagnosed within 5 years of childbirth impart a ∼3-fold increased risk for metastasis compared with breast cancers diagnosed in age-matched nulliparous or pregnant women ( 1–3). This article is highlighted in the In This Issue feature, p. We identify a previously unrecognized biology, namely weaning-induced liver involution, that establishes a prometastatic microenvironment, and which may account in part for the poor prognosis of patients with postpartum breast cancer. Significance: We find that patients with postpartum breast cancer are at elevated risk for liver metastasis.
In sum, our data reveal a previously unknown biology of the rodent liver, weaning-induced liver involution, which may provide insight into the increased liver metastasis and poor prognosis of women diagnosed with postpartum breast cancer.
Human relevance is suggested by a ∼3-fold increase in liver metastasis in patients with postpartum breast cancer ( n = 564) and by liver-specific tropism ( n = 117). Using intracardiac and intraportal metastasis models, we observed increased liver metastasis in post-weaning BALB/c mice compared with nulliparous controls. Upon weaning, we observed liver weight loss, hepatocyte apoptosis, extracellular matrix remodeling including deposition of collagen and tenascin-C, and myeloid cell influx, data consistent with weaning-induced liver involution and establishment of a prometastatic microenvironment. Here, we address whether circulating tumor cells have a metastatic advantage in the postpartum host and find the postlactation rodent liver preferentially supports metastasis.
Patients with postpartum breast cancer are at increased risk for metastasis compared with age-matched nulliparous or pregnant patients.
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