Abstract:

Breast cancer and other malignities occur as a result of genetic changes that affect the cell pathway involved in cell growth and development. Proto-oncogens contain codes of some proteins that are important for normal cell growth and differentiation. If a mutation results in a change in the structure of the proto-onkogenin, the damage that occurs, by changing the attachment of the gene and gene product, eliminates the control of cell division in various ways and malignité occurs. In the formation of cancer, a second important group of genes in addition to oncogens are also tumor-pressing genes. The fate usually interact with one another in a homophistic character and connects the cell-cell adhesion. Due to the irregular behavior of tumor cells, the cell-cell relationship in the tumors is deteriorated. E-Caderin (CDH-1) causes the cell’s mobility property to disappear. In breast cancer, the epithelium cells gain mobility due to loss of expression of E-Caderin or disorder in the phosphorylation of the cytoplasmic part, and an increase in local spread is observed. The lack of E-Cader is responsible for the appearance of invasive phenotypes and leads to poor forecast in dyctal carcinomas. Matrix metalloproteinase (MMP) gene family extrasellules are nine or more endopeptidase codes that show activity against matrix macromolecules. Studies have shown that increased MMP-3 expression in breast cancer is promoting the tumor prognosis. In light of this information, our study aimed at studying the effects of E-Caderin -160 C/A and MMP-3 5A/6A gen polymorphisms on breast cancer. For this purpose, we used the method of length polymorphism (PZR-RFLP) for determining relevant gen polymorphisms in our study. As a result of the statistical assessment, we got the impression that the MMP-3 6A allel and E-Cader can play a role in the development of the disease and the formation of metastases.

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