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EN
The aim of the study was to determine the localization of estrogen receptors α in the parahippocampal gyrus (gyrus parahippocampalis) following 17β application in ovariectomized rabbits. Studies were carried out using an immunocytochemical method. Estrogen receptors a immunoreactivity in neurons and astrocytes were detected in the cellular layers of parasubiculum, perisubiculum and entorhinalis region. However ERα immunoreactivity was not detected in astrocytes ovariectomized rabbits in the experimental group where there was no E2 application. On the other hand, the neurons showed very weak colorization. The results obtained indicate that the structure of rabbit parahippocampal gyrus is under the influence of estrogen, which causes an increase in ERα expression.
EN
The study aimed at monitoring the expression of oestrogen (ER) and progesterone (PGR) receptors in mammary gland adenocarcinomas in bitches as compared to the mitotic activity of the neoplastic cells. Material for the study involved samples of mammary tumors obtained during surgery from 48 bitches of various races, aged 7 to 15 years. The obtained preparations were microphotographed and the patterns were subjected to computer-assisted image analysis in a system consisting of a computer linked to an Axiophot light microscope (Carl Zeiss). The expression of ER, PgR and of Ki-67 was evaluated using a semi-quantitative scale which involved evaluating the proportion of positive cells (0-5% no reaction [], 6-25%: weak reaction [+], 26-50%: moderate reaction [++], above 50%: intense reaction [+++]). The evident deficit of ER observed in our studies might indicate an oestrogen independency of the adenocarcinomas in bitches. This, however, does not preclude involvement of the receptors at earlier stages of carcinogenesis. The obtained strong correlation between expressions of Ki-67 and that of PgR (r=0.67), in view of the high prognostic value of Ki-67 expression, confirmed in numerous studies, allow the conclusion that presence of progesterone receptors in the cells of mammary gland adenocarcinoma in bitches is linked to the augmented proliferative potential of the tumors, similarly as it has been demonstrated in mammary glands in females.
Medycyna Weterynaryjna
|
2010
|
tom 66
|
nr 11
s.745-750,fot.,rys.,bibliogr.
EN
The aim of this article is to summarize current data on the role of growth factors in the development of mammary tumors and their receptor expression as tumor markers. Particular attention is paid to IGF-I and IGF-IR in canine mammary tumors. The growth of a canine and human mammary cancer is regulated not only by sex steroid hormones but also by growth factors (GFs). Growth factors control such critical processes as the growth of the cell, differentiation, angiogenesis and apoptosis in a normal mammary gland. In malignancies these signaling pathways are often exploited to stimulate tumor growth and metastasis. In recent years there has been an increased understanding of aberrations in the insulin-like growth factor-I and its receptor (IGF-I, IGF-IR) responsible for or accompanying human and canine mammary carcinogenesis. IGF-IR demonstrates a tyrosine kinase activity and closely resembles the insulin receptor (IR) in structural as well as in signaling cascades. The binding of the ligands IGF-I or IGF-II to IGF-IR causes the phosphorylation of the IGF-IR tyrosine kinase rest located in the cytoplasmic portion of the β-subunit, then the Ras/ MAPK and PI-3K/Akt pathways associated with cell differentiation are activated and apoptosis is inhibited. IGF-IR is overexpressed in mammary tumor cells and has been implicated in tumor aggressiveness. IGF-IR expression contributes to cancer cell migration as well as cell-cell adhesion. The assessment of IGF-IR expression seems to be a significant indicator of prognosis. There are only a few studies on the role of IGF-I/IGF-IR in canine mammary neoplasms. Interestingly, the cross-talk between estrogens/ERα and IGF-I/IGF-IR has been demonstrated in breast cancer. Most in vitro studies demonstrate that estrogens and IGF-I have a synergistic effect on the proliferation of breast cancer cells. In the case of canine mammary tumors this potential relationship has not been thoroughly investigated, but it has been hypothesized that such a mechanism of cross-talk between sex hormones and the IGF-I pathway might promote carcinogenesis in an autocrine/paracrine manner. A further understanding of this mechanism could lead to the development of new therapeutic strategies in canine and human mammary neoplasms.
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