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Mitotic figures are frequent, disperse or in line, throughout the breast stroma.
Small cells infiltrating breast stroma surrounding benign breast tissues in a targeted manner.
These increased ductal secretions may lead to damaged ductal epithelium with glandular secretions leaking into the connective tissue of the breast stroma.
Current theories of IGM etiology favor an inflammatory response within the connective tissue of breast stroma to glandular secretions leaked from damaged ductal epithelium [2].
Histologically, they arise from the intralobular breast stroma and tend to form cords that extend into adjacent normal breast parenchyma, a characteristic that simulates the growth pattern of infiltrating carcinoma [25, 26, 27].
To illustrate the statistical issues involved we discuss three microarray studies related to the microenvironment and tumor biology involving: (i) prostatic stroma cells in cancer and non-cancer tissues; (ii) breast stroma and epithelial cells in breast cancer patients and non-cancer patients; and (iii) serum associated with wound response and stroma in cancer patients.
We identified three mesenchymal/stromal-signatures which A17 cells shares with MSCs and breast stroma.
Small ALDH1 positive cells were also found in normal breast stroma (Figure 1B).
Accordingly, breast stroma samples, MSCs and breast organelle expressed the highest values of COX-2 (Figure 3d).
This is important, and supports the increasingly accepted concept that the stromal tissue that is part of the tumour may phenotypically be distinct from the normal breast stroma.
However, as far as we are aware, nobody has shown that its expression is restricted to breast stroma and MSCs and can identify breast cancer mesenchymalization.
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