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The aim of the research was to show the immunocytochemical expression of MT and Ki-67 and the correlation between these markers in spontaneous epithelium mammary gland cancer in bitches. The samples used in the research were extracted during surgical procedures from 20 bitches of different breeds, ranging from 6 to 15 years of age who had been diagnosed with mammary gland tumors. The prepared samples were then photographed with a microscope, to be later analyzed by a workstation comprised of a computer hooked up to a Carl Zeiss microscope model: Axiophot. The workstation was able to register images and then digitally analyze them. The MultiScaneBase V 8.08 program working on a Microsoft Windows platform was used to gather readings. The average correlation value between the Ki-67 and MT expression confirmed by many tests indicated a high index value of Ki-67 antigen as the prognostic agent. The study concluded that the presence of metalotionein in adenocarcinamas of the mammary gland in bitches does not indicate its connection with an increased proliferation potential of the cancer cells as is in the case in womens mammary gland tumors.
Medycyna Weterynaryjna
|
2010
|
tom 66
|
nr 11
s.745-750,fot.,rys.,bibliogr.
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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