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Abstract Breast cancer is the most common cancer and the second most common cause of death in women. It is an ancient and elusive disease, which has claimed its many victims through the world. Breast cancers have been show to elicit tumorspecific immune responses. Despite expression of tumorassociated antigens the presence of tumorspecific cytotoxic T lymphocytes the immune system fail to contain breast carcinoma. Recent evidence suggests that cellmediated immunity in different tumors may be down regulated through programmed cell death (apoptosis) pathways. An alternative mechanism of apoptosis is through the activation of death receptors on the cell membrane. The archetype of this molecular system is Fas (Apo1, CD95), a cellsurface receptor that is a member of the tumor necrosis factor. By ligation of Fas ligand (FasL) Fas induce apoptosis on various type of cells. Bcl2 belongs to a new category of oncogenes that acts by overriding programmed cell death, thus favoring a prolonged survival of normal and neoplastic cells. Other factor that inhibit apoptosis the transcription factor NF B which is a regulator of genes encoding cytokines, cytokine receptors, and cell adhesion molecules that drive immune and inflammatory responses. So, this study was suggested to find the mechanism by which breast cancer inhibit and evade antitumor immune response by evaluating the role of apoptotic process in lymphocyte inhibition. METHODS: The morphological feature of apoptosis were assayed microscopically, serum levels of apoptosis related proteins (Fas, FasL, Bcl52 and NF B) were assayed by ELISA in addition genes of the last protein were assayed using RTPCR technique. CONCLUSION: It can be concluded that, tumorinduced apoptosis of lymphocytes may combine the engagement of various apoptotic stimuli and pathways. In addition, this study determined new immune therapy strategies of controlling evading antitumor immune response that might be potential targets for therapeutic intervention in the future. The enhancement of lymphocyte survival rate by the activation of the programmed cell death inhibitors namely Bcl2 and NF B and inhibit its inducers namely Fas/FasL system may be one of these strategies. Furthermore, patients with breast cancer can follow up via nonenvasive biochemical techniques including measurements serum sFas, sFasL, Bcl2 and NF B. |