Abstract
The human breast comprises three lineages: the luminal epithelial lineage, the myoepithelial lineage, and the mesenchymal lineage. It has been widely accepted that human breast neoplasia pertains only to the luminal epithelial lineage. In recent years, however, evidence has accumulated that neoplastic breast epithelial cells may be substantially more plastic in their differentiation repertoire than previously anticipated. Thus, along with an increasing availability of markers for the myoepithelial lineage, at least a partial differentiation towards this lineage is being revealed frequently. It has also become clear that conversions towards the mesenchymal lineage actually occur, referred to as epithelial to mesenchymal transitions. Indeed, some of the so-called myofibroblasts surrounding the tumor may have an epithelial origin rather than a mesenchymal origin. Because myoepithelial cells, epithelial to mesenchymal transition-derived cells, genuine stromal cells and myofibroblasts share common markers, we now need to define a more ambitious set of markers to distinguish these cell types in the microenvironment of the tumors. This is necessary because the different microenvironments may confer different clinical outcomes. The aim of this commentary is to describe some of the inherent complexities in defining cellular phenotypes in the microenvironment of breast cancer and to expand wherever possible on the implications for tumor suppression and progression.
Highlights
Human breast cancer cells are generally believed to originate from the luminal epithelial lineage of terminal duct lobular units [1]
This is important because it allows for possible strategies to influence the breast cancer cells towards a more differentiated state
The growing number of myoepithelial markers is providing evidence that neoplastic breast cancer cells frequently exhibit at least a partial myoepithelial differentiation program [8,9,10]
Summary
Human breast cancer cells are generally believed to originate from the luminal epithelial lineage of terminal duct lobular units [1]. It has been shown that loss of differentiation in breast cancer, invasion and metastasis both in vivo and in culture concur with epithelial to mesenchymal transition (EMT) of the tumor cells [16,17,18,19,20,21]. The concept of direct EMT is used to explain the phenotype of very aggressive metastatic cells to the bone marrow [50] These cells express vimentin in conjunction with luminal epithelial markers [50]. There is no unequivocal correlation between gain of vimentin or loss of E-cadherin expression and poor prognosis [16,52] One explanation for this could be that some of the cases with vimentin-positive cells and E-cadherin-negative cells reflect myoepithelial differentiation rather than direct EMT from luminal epithelial cells. A consequence of a possible evolutionary relationship between the stroma and the neoplastic lesion remains to be seen
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