Abstract
Breast cancer is unique among cancers in that its growth is strongly regulated in about one third of clinical cases by estrogenic hormones or antiestrogenic antagonists (1). Breast cancer occurs in women who never had functional ovaries with only 1% of the frequency of that in women with intact ovaries. Thus, estrogens are stimulatory, at least initially, in nearly all breast cancers. This hormonal component of growth control appears to be a remnant of normal, differentiated epithelial proliferation. During puberty or pregnancy-lactation, estrogen exerts mitogenic, anabolic and secretory effects on mammary epithelium. While estrogen is a proximate mitogen for either normal or malignant breast epithelium, the hypothalamus-pituitary axis is indirectly in control of ovarian estrogen secretion by virtue of gonadotropin releasing hormone and gonadotropin stimulation (2).
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Abbreviations
- E2 :
-
estradiol
- IMEM:
-
improved nodified Eagle’ medium
- CM:
-
conditional meduim
- CME2 :
-
medium conditioned by cells petreated with estradiol
- HPLC:
-
high performance liquid chromotography
- PDFG:
-
platelet-derived growth factor
- EGF:
-
epidremal growth factor
- IGF:
-
insulin-like growth factor
- TGF:
-
transforming growth factor
- FGF:
-
fibrolast growth factor
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Dickson, R.B., Lippman, M.E. (1987). Regulation of Growth and Secretion of Growth Factors by 17 B-Estradiol and V-RASH Oncogene in Human Mammary Carcinoma Cell Lines. In: Medina, D., Kidwell, W., Heppner, G., Anderson, E. (eds) Cellular and Molecular Biology of Mammary Cancer. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0943-7_13
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