Post-lactational mammary gland regression: molecular basis and implications for breast cancer
|Christine J. Watson a1
a1 Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK. Tel: +44 (0)1223 333725; Fax: +44 (0)1223 333346; E-mail: firstname.lastname@example.org
During pregnancy, there is a massive increase in the number of luminal epithelial cells in the breast, which are destined to become the milk factories after birth. These cells are no longer required when the young are weaned, and are removed in a carefully orchestrated event called involution. In this process, the secretory epithelial cells die and are replaced by adipocytes, which redifferentiate as the epithelium is removed. It is essential that the gland is properly remodelled to a pre-pregnant state so that successful lactation can occur following a subsequent pregnancy. Furthermore, failure to remove unnecessary lactational alveoli during weaning could result in inflammation and tissue damage. Recently, it has been shown that components in the fatty stroma in involuting breast can promote metastasis. Thus, it is important to understand the molecular mechanisms that regulate involution, how these can fail, the consequences of the remodelling process, and how this knowledge can inform us about breast cancer. In this review, I discuss the roles of the JAK–STAT, NF-κB and other signalling pathways in the regulation of apoptosis and tissue remodelling during involution.