Abstract
Specification of mammary epithelial cell fate occurs during embryogenesis as cells aggregate to form the mammary anlage. Within the embryonic mammary bud, a population of epithelial cells exists that will subsequently proliferate to form a ductal tree filling the stromal compartment, and which can produce milk upon terminal differentiation after birth. Subsequently, these structures can be remodelled and returned to a basal state after weaning before regenerating in future pregnancies. The plasticity of the mammary epithelial cell, and its responsiveness to hormone receptors, facilitates this amazing biological feat, but aberrant signalling may also result in unintended consequences in the form of frequent malignancies. Reflecting this intimate connection, a considerable number of signalling pathways have been implicated in both mammary gland morphogenesis and carcinogenesis.
Highlights
Like many other organs, mammary glands are formed by an exchange of signals between epithelia and mesenchyme [1,2,3]
The fundamental processes required for the inductive events of mammary bud development are those that are perturbed in breast cancers [9,10]
This study showed that during early mammary bud development the interaction of Tbx2 and Tbx3 is mediated via a p19Arf/p53-independent pathway
Summary
Mammary glands are formed by an exchange of signals between epithelia and mesenchyme [1,2,3]. It is unknown precisely how the mammary phenotype is conferred, but it appears that mesenchymal signals cause local migration of epidermal cells to form the mammary anlage rather than via localised proliferation [4,5,6]. The fundamental processes required for the inductive events of mammary bud development (epithelial migration, changes in cell adhesion, growth, death, and differentiation) are those that are perturbed in breast cancers [9,10].
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