The epithelial component of normal and noninvasive breast tumor tissue is physically separated from the stroma by both the myoepithelial cells and the basement membrane (BM). Myoepithelial cells are joined by intermediate or gap junctions and a number of intercellular adhesion molecules, forming a continuous sheet or belt that encircles the epithelial cells (except at the terminal ductal-lobular unit, within which about 20% of the epithelial cells are reported to be in direct contact with the BM) BM = basement membrane; DCIS = ductal carcinoma in situ; ER = estrogen receptor; H & E = hematoxylin and eosin; LOH = loss of heterozygosity; MI = microsatellite instability; PCR = polymerase chain reaction; SMA = smooth muscle actin. AbstractIntroduction Our previous studies detected focal disruptions in myoepithelial cell layers of several ducts with carcinoma in situ. The cell cluster overlying each of the myoepithelial disruptions showed a marked reduction in or a total loss of immunoreactivity for the estrogen receptor (ER). This is in contrast to the adjacent cells within the same duct, which were strongly immunoreactive for the ER. The current study attempts to confirm and expand previous observations on a larger scale.

The seven signal transducer and activator of transcription (STAT) molecules are effectors of hormonal or cytokine stimulation through receptors. STAT 5a, isolated from prolactin-stimulated mammary cells, contributes to normal proliferation and is essential for mammary gland differentiation. Using a monoclonal antibody, we tested 100 formalin-fixed, paraffin-embedded breast tissues representing everything from simple hyperplasia to invasive carcinoma for the expression of STAT 5a in comparison to normal breast epithelial cells. Immunohistochemical analysis was performed following heat treatment in a pressure cooker. STAT 5a was found in endothelial cells, adipocytes, and leukocytes as well as in the cytoplasm and nucleus of normal epithelial cells, usual ductal hyperplasia, and benign lesions such as fibroadenoma. Myoepithelial cells and stromal fibroblasts failed to demonstrate any STAT 5a in addition to most atypical proliferations including in situ and invasive carcinomas. A few examples of lobular intraepithelial neoplasia and invasive carcinoma demonstrated some reactivity, albeit comparatively reduced. The absence of STAT 5a in the abnormal breast epithelial cells may indicate a defect contributory to the abnormal state.

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