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Background malignant lymphoma (malignant lymphoma, ML) is primary in the lymph nodes or extranodal tissue is a malignant cancer of the lymphatic or organ comes from the malignant transformation of lymphocytes or tissue. 7 of the rankings for all cancer in developed countries, ML, in developed countries for the first nine, the rankings of the world's total of nine. And parts of the world, China is a low-incidence areas. Around the world have shown that the incidence of non-Hodgkin's lymphoma showed a continuing upward trend in age, from childhood to the age of 80 in developed countries age section for men 60-70 years old, women 70-74 years of age However, in developing countries, young people accounted for a very high ratio. Various subtypes different than in the composition of the different ages and adult B-cell non-Hodgkin's lymphoma (B-Cell NHL) accounted for 85%, about 15% of T-Cell NHL; children the B-CellNHL accounted for 35%, T-Cell NHL accounted for 65%; Burkitt lymphoma, lymphoblastic more occur in children. Tumorigenesis is a multi-factor, multi-step development process is the result of the interaction of multiple genes. Cell proliferation, differentiation and apoptosis of cells are the basic activities of life, three are closely related. Normal cell proliferation, differentiation and apoptosis by strict regulation, any link to a problem may lead to imbalance between these three, which led to the occurrence of malignant tumors, development of a series of complex gene cluster. Apoptosis is one of the fundamental features of life, and the regulation of apoptosis disorders contribute to malignant transformation and tumor progression. Bcl-2 is the first to be found apoptosis suppressor gene by Tsujimoto et al 1984 study of human follicular lymphoma found. Normal circumstances, Bcl-2 gene is located on human chromosome 18q21, is composed of three exons encoding 239 amino acids consisting of a molecular weight of 26Kb of Bcl-2 protein. Bcl-2 gene rearrangement of chromosomal translocation t (14; 18) the result of normal and translocation alleles were expressed in a membrane-bound protein, and positioning in the mitochondrial membrane, has the role of blocking apoptosis. Livin newly discovered IAPs (apoptotic protein inhibiting factor) family members, also known as ML-IAP or KIAP found so far the strongest inhibitor of apoptosis, one of the factors mainly through direct inhibition of caspase-3 activated to block death receptor and mitochondrial-based apoptotic pathway. Smac is equal to the first report in July 2000 by Wang, a novel mitochondrial proteins isolated from HeLa cells, named for the second mitochondria-derived cysteine ??protease activation agent (second mitochondrial-derived activator of of caspase, Smac ). Smac relieve IAP inhibition of caspase-9, 3,7, etc. combined with each other and members of the IAP family, activation of caspase cascade, promote apoptosis. Objective: To investigate the apoptosis inhibitory gene Bcl-2 expression of Livin and pro-apoptotic gene Smac in B-Cell NHL, the relationship between the expression of the three B-CellNHL clinical prognostic factors. Methods: Immunohistochemistry was detected 40 cases of B-Cell NHL, 15 patients with lymph node reactive hyperplasia, Bcl-2, Livin and Smac expression. Results: Bcl-2, the positive expression rates of Livin in B-Cell NHL were 62.5% and 65%, and its rate of positive expression in lymph node reactive hyperplasia (26.7%, 20%), the difference was statistical significance (P <0.05); Smac in B-Cell NHL group the positive rate was 60%, compared with 80% positive rate of lymph node reactive hyperplasia group, the difference was not statistically significance (P = 0.165> 0.05); expression of Bcl 2 and Livin expression in B-Cell NHL was a positive correlation (r = 0.731, P <0.001); Bcl-2 was negatively correlated with the expression of Smac both (r = -0.316, P <0.05); of Livin and Smac the both expression was positively correlated (r = 0.364, P <0.05); B-Cell NHL, Bcl-2, expression of Livin expression was correlated with the patient's gender, age, AnnArbor staging (P> 0.05) of Smac positive expression and sex of the patient, regardless of age (P> 0.05), and AnnArbor installments related (P <0.05). Conclusion: B-Cell NHL in Bcl-2 and Livin may act synergistically to inhibit tumor cell apoptosis; Bcl-2 and Smac may play an antagonistic role in the regulation of apoptosis; of Livin and Smac in B-Cell NHL may play a synergistic role in the occurrence and development.
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