“…[58][59][60] In fact, studies have shown that expression of TfR is more abundant in breast cancer tissue than in normal tissue. 60,61 Given the facts that estrogen and Fe exert their biological effects through their receptors, 62,63 it is important to know whether E2 affects TfR in cells with different ER and PR status.…”
Estrogen and iron play critical roles in a female body development and were investigated in the present study in relation to in vitro cell proliferation. Prempro™, a hormone replacement therapy drug, and 17β-estradiol (E2) were shown to increase cell proliferations in estrogen receptor positive (ER + ) cells independent of progesterone receptor (PR) status. For example, increased cell proliferation was observed in ER + /PR + human breast cancer MCF-7, its matching non-cancerous human breast epithelial MCF-12A, and ER + /PR + murine mammary cancer MXT + cells, but not in ER − /PR − MDA-MB-231, its matching non-cancerous MCF-10A, and MXT − (ER − /PR + ) cells. By mimicking post-menopausal conditions of high estrogen in local breast tissue and increased iron levels due to cessation of menstrual periods, E2 and iron were shown to exert synergistic effects on proliferation of MCF-7 cells and significantly increased Ki67 and proliferating cell nuclear antigen. Western blotting of E2-treated ER + but not ER − cells showed that E2 also increased transferrin receptor (TfR). Further studies are needed to assess the mitogenic effects of iron and estrogen in normal post-menopausal breast.
“…[58][59][60] In fact, studies have shown that expression of TfR is more abundant in breast cancer tissue than in normal tissue. 60,61 Given the facts that estrogen and Fe exert their biological effects through their receptors, 62,63 it is important to know whether E2 affects TfR in cells with different ER and PR status.…”
Estrogen and iron play critical roles in a female body development and were investigated in the present study in relation to in vitro cell proliferation. Prempro™, a hormone replacement therapy drug, and 17β-estradiol (E2) were shown to increase cell proliferations in estrogen receptor positive (ER + ) cells independent of progesterone receptor (PR) status. For example, increased cell proliferation was observed in ER + /PR + human breast cancer MCF-7, its matching non-cancerous human breast epithelial MCF-12A, and ER + /PR + murine mammary cancer MXT + cells, but not in ER − /PR − MDA-MB-231, its matching non-cancerous MCF-10A, and MXT − (ER − /PR + ) cells. By mimicking post-menopausal conditions of high estrogen in local breast tissue and increased iron levels due to cessation of menstrual periods, E2 and iron were shown to exert synergistic effects on proliferation of MCF-7 cells and significantly increased Ki67 and proliferating cell nuclear antigen. Western blotting of E2-treated ER + but not ER − cells showed that E2 also increased transferrin receptor (TfR). Further studies are needed to assess the mitogenic effects of iron and estrogen in normal post-menopausal breast.
“…Creatinine plays an important pathophysiological role in the cyst development [94]. The peculiar accumulation of ferritin and transferrin [112,122], plasminogen [135], b-thromboglobulin and thrombospondin [134,137] in Type I gross cysts has been suggested as clinical useful tool to distinguish the high biosynthetic activity of the apocrine 'metaplastic' cells, pathophysiologically linked to an active and selective accumulation process against a concentration gradient [137]. Among cell-adhesion molecules, only endothelin-1, ICAM-1, VCAM-1 and E-selectin have been reported occur in higher concentrations in apocrine Type I respect to flattened GCBD [119,130], suggesting a pathogenetic function mediated through paracrine/autocrine mechanisms [121], modulated in part by interleukins [130].…”
For more than one and a half century the cystic disease of the breast has been recognized as the most frequent female benign breast lesion. Although some conundrums and controversies exist about the relation between gross cysts and breast cancer, recent evidence suggests that the multidisciplinary study of gross cystic breast disease (GCBD) may be a powerful tool for predicting the natural history of the multifaceted gross cyst pathology. A lot of papers have been published on breast cyst fluids (BCF) concerning biochemical, hormonal and morphological aspects, demonstrating that the intracystic fluid contains a wide variety of components (such as ions, lipids, proteins, enzymes, growth factors and antigens) and suggesting that their profile provides additional knowledge on both physiopathology and etiologic pathways of human gross cystic breast disease. The aim of this overview is the critical evaluation of all data accumulated in the last thirty years, in order to highlight the utility of biochemical and epidemiological studies to identify gross cysts, if any, at higher breast cancer risk.
“…Riskli katyon oranı (Na/K 2'nin altında) veren kistlerin postmenopozal gruba kıyasla premenopozal hastalarda daha sık görüldüğü belirlenmiştir (3).…”
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