الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Breast cancer the most common cancer in women worldwide, with nearly 1.7 million new cases diagnosed in 2012 (second most common cancer overall). This represents about 12% of all new cancer cases and 25% of all cancer in woman. In Arab countries. Approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells.
Epithelial-mesenchymal transition (EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development. Tumor cells usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. Several transcription factors and signals are involved in these events.
It is well known that the E-cadherin/β-catenin complex is very important in maintaining epithelial morphology. This complex maintains integrity of epithelial cell-cell contact and keeps Wnt/β-catenin signals in check. Loss of cadherin-mediated cell adhesion can promote β-catenin signaling, and high-affinity E-cadherin/β-catenin interaction can be disrupted during oncogenesis and fibrosis.
Loss of E-cadherin expression or loss of its normal localization at cell-cell contacts is consistently observed at sites of EMT during tumor progression. E-cadherin expression level is often inversely correlated with the tumor malignancy. Cancer studies suggest that deregulated β-catenin signaling promotes tumor genesis by inducing expression of oncogenes such as c-myc and cyclin D1. Stabilizing mutations in the β-catenin N-terminal sequence have been found in 25% of metaplastic breast cancers. Increased cytoplasmic and nuclear β-catenin levels have been observed in 40% of primary breast cancers and correlated with poor prognosis and worse patient survival.
Numerous theories have been put forward to define the role of vimentin in pathogenesis of breast carcinomas. Initially, epithelial mesenchymal transition of tumor cells was thought to be the mechanism of vimentin expression. Alternatively, vimentin expressing breast carcinoma cells may be derived from breast progenitor cells with bilinear (glandular and myoepithelial) differentiation potential and not because of epithelial mesenchymal transition.
The current work was designed to study the immunohistochemical expression of E-cadherin, β-catenin and vimentin as EMT markers