In the reproductive age of nulliparous women, the epithelium of the breast is subjected to cyclic cell proliferation and subsequent apoptosis (spontaneous programmed cell death), which are a consequence of the cyclic function of the ovaries. Cyclic changes in the levels of sex steroid hormones during the menstrual cycle significantly affect the morphofunctional state of the mammary glands.

Hormones of the ovaries (estrogens, progesterone, androgens) have mainly a stimulating effect on the proliferation and differentiation of mammary gland cells.

In the follicular phase of the menstrual cycle under the influence of estrogens, cell proliferation takes place in the terminal sections of the ducts, and luteal phase is provided by the lobular alveolar development and cellular differentiation due to the action of progesterone.

Russo and I. Russo (I996) distinguish three main mechanisms of the proliferative effect of estrogens on the mammary gland:.

direct stimulation of cell proliferation due to the interaction of estradiol, associated with nuclear estrogen receptors;.

mediated stimulation due to the induction of the synthesis of growth factors both autocrine and paracrineally acting on the epithelium of the mammary gland;.

oppression estrogen secretion of biologically active substances, inhibiting growth factors in the mammary gland.

In addition to estrogens, the proliferation and differentiation of epithelial MF cells is stimulated, and the following growth factors and protooncogenes are inhibited by apoptosis (Russo I. , Russo I. , 1996):.

epidermal growth factor;.

insulin-like growth factors of type 1 and II;.

a-transforming growth factor;.

protooncogenes c-fox, c-mix, c-jun.

Progesterone supports cyclic proliferation of mammary glands in the normal menstrual cycle, as well as during pregnancy, and its main role is to stimulate the development of alveoli. In women with a regular cycle, the maximum proliferation of mammary epithelial cells is set in the luteal phase against a background of high levels of progesterone. Perhaps this is why the maximum size of mammary glands is observed in the late luteal phase of the cycle. However, it should be noted that the peak of mitosis in the luteal phase is replaced by apoptosis.

If estrogens increase the size of the ducts of the gland by hypertrophy of the lining cells, then progesterone causes hyperplasia of these cells by increasing the chemical activity of pre-lactation compounds in the terminal ducts.

In the luteal phase, the number of estrogen receptors decreases in the mammary epithelium, while the number of progesterone receptors remains high throughout the cycle.

Thus, progestogens:.

stimulate growth, but do not stimulate the cell proliferation of the mammary gland;.

reduce the number and reduce the expression of estrogen receptors, thereby inhibiting estrogen-induced mitoses;.

reduce the production of proto-oncogenes, such as c-tus and c-fos (Wren B. , 1995);.

reduce the production of cathepsin D - the active growth factor of cancer cells (Wren B. , 1995).

When pregnancy occurs, the effect of the placenta produced by the placenta is chorionic gonadotropin (HG), prolactin, and also the hormone of the yellow body - progesterone. During this period, the synthesis of pituitary hormones decreases and the production of prolactin-inhibiting factor in the hypothalamus.

In the works I. Russo and 1. Russo (1998) showed that human CG produced during pregnancy has a protective effect on breast tissue. Thus, CG can have a direct effect on the epithelium of the mammary gland by inhibiting cell proliferation, and also due to the paracrine influence to stimulate the synthesis of breast tissue by inhibin, which influences cell proliferation by activating a gene that controls the cell cycle and apoptosis.

Under the influence of HG, the structural changes in the mammary gland cells that can occur under the influence of carcinogenic agents.

Direct antiproliferative effect of CG on epithelial cells is due to:.

enhancing DNA recovery;.

reduce carcinogen-DNA binding;.

activation of apoptosis;.

oppression of cell growth.

In an animal experiment, the protective effect of HG on the mammary gland was shown in an attempt to cause cancer by chemical carcinogens. Consequently, the use of HC in the clinic can potentially be included in the complex of prevention and therapy of breast tumors. However, this method is currently only entering the phase of clinical trials and recommendations on this subject in the literature there. Nevertheless, the above-mentioned information again explains the oncoprotective effect on the mammary gland of pregnancies, labor and lactation.

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