Mammary Stem Cell Reprogramming and Breast Cancer

Dear Colleagues,

Alterations in mammary development have been associated with modified breast cancer risk for decades. The underlying mechanisms, however, remain unclear. Recent breakthroughs in stem cell technology, functional genomics, and epigenetics have significantly advanced our understanding of the role of mammary stem and progenitor cells in the transition of the critical stages of mammary development, which include prenatal, pre-pubertal, post-pubertal, adult resting gland, pregnancy, lactation, and involution stages. Increasing evidence supports mammary stem/progenitor cells as the cell-of-origin in many breast cancers. In particular, mammary stem and progenitor cells are sensitive to genetic/epigenetic, hormonal, dietary, and environmental factors. The influence from these factors, especially during the critical stages, may “reprogram” mammary development and lead to physiological or tumorigenic consequences. The changes in mammary stem cell repopulation and dynamics are accompanied by the activation of a plethora pathways, such as Wnt and Notch signaling. Therefore, elucidating the mechanism of mammary stem cell reprogramming and identifying the factors that modulate this process are critical to advancing our understanding of breast cancer etiology and developing targeted chemoprevention strategies against breast cancer. To follow the increasing studies on mammary reprogramming, we have organized the current Special Issue to accept original studies, reviews, and technical reports on different aspects of mammary stem cell reprogramming and breast cancer risk. Topics of interest include, but are not limited to, identification of novel markers of mammary stem and progenitor cells; understanding the genetic and epigenetic regulation of mammary stem cells; delineating the signaling pathways in mammary stem cell regulation; perinatal and pubertal exposure to hormonal, dietary, and environmental factors on breast cancer risk later in life; regulation of stemness, such as the epithelial-to-mesenchymal transition (EMT), in mammary stem cell reprogramming; comparative studies of mammary stem cells with human breast cancer stem cells; and regulation of apoptosis and autophagy in glandular remodeling. We expect the reports in this Special Issue to facilitate the “decoding” of mammary stem cell reprograming in development and tumorigenesis, which could be applied to breast cancer prevention and treatment. We are looking forward to your contributions to this Special Issue. 

Dr. Xiaohe Yang
Guest Editor

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• breast cancer etiology
• mammary stem cells
• mammary reprogramming
• cancer stem cells
• hormonal modulation
• targeted chemoprevention
• EMT
• apoptosis