الفهرس 
Introduction and Aim of the workOnly 14 pages are availabe for public view
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Abstract
Breast cancer is a common malignancy among women, whose development and progression were extensively investigated, at the basic and clinical levels. The intensive research has led to the understanding that a large variety of intrinsic properties of the tumor cells dictates together with host factors the course of disease. Breast cancer in the population probably results from complex interactions between many genetic and environmental factors over time. Cumulative lifetime exposure to estrogen, estrogen metabolites, and other physiological factors, as well as environmental exposures, could play an important role in the etiology of breast cancer.
A number of studies have evaluated possible associations between a polymorphism in CYP17 gene and breast cancer risk. CYP17 functions at key branch points in human steroidogenesis. The role of the MspA1 genetic polymorphism in the 5′region of CYP17 on risk of breast cancer was investigated and as a modifier of reproductive risk factors.
As in other malignant diseases, major emphasis was put on the roles played by constituents of the tumor microenvironment in breast malignancy, giving noteworthy attention to inflammatory mediators :
cells, cytokines and chemokines. Chemokines were shown to affect malignancy in various ways, either promoting or inhibiting tumor growth and metastasis formation Specifically in breast cancer, many investigators focused on the inflammatory chemokines, IL1α, CCL5 and TNFα Steroid hormones exert growth - promoting effects and induce breast cell proliferation by binding to intracellular receptors and regulating gene transcription. Experimental data strongly suggest that estrogens have a