The Study Of The Expression Of Bcl-2,Livin And Smac And The Relationship Between Them In B-cell Non-Hodgkin's Lymphoma

Background:Malignant lymphoma (ML) is a malignant tumor which primarily developed from lymph nodes or tissues or organs outside the lymph nodes and derived from lymphocytes or malignant cells . ML ranked No.7 in all malignant tumors in developed countries, No.9 in developing countries, and No.9 in the overall ranking of the world. Compared with some parts of the world, China had a low incidence. Information around the world had shown that the incidence of non-Hodgkin's lymphoma continued upward with age. from childhood to 80 years old, developed countries had a high incidence of male 60-70 years old, for female 70-74 years old. However,in developing countries young people relatively had a high ratio.different age group had it's subtypes. Among the adult people B-cell non-Hodgkin's lymphoma (B-Cell NHL) accounted for 85% and T-cell NHL accounted for about 15%. While among children B-Cell NHL accounted for 35% and T-Cell NHL accounted for 65%; Burkitt lymphoma, lymphoblastoid cell NHL occurred in children much more ofen.Tumorigenesis is a multi-factors, multi-steps process, is the result of the combined effect of genes . Cell proliferation, differentiation and apoptosis are the cell's basic life activities,and they are closely related. The proliferation, differentiation and apoptosis of normal cell are strictly regulated by a series of complex gene cluster, anyone of them goes wrong may lead to a disbalance between the three, which could lead to the occurrence and development of malignant tumors. Apoptosis is one of the fundamental features of life, and disordered regulation of apoptosis may contribute to the malignant cell transformation and tumor progress . Bcl-2 is the first found inhibitor of apoptosis gene, and was detected in human follicular lymphoma in 1984 by Tsujimoto and others. Bcl-2 gene locates in human chromosome 18q21, has 3 exons, encodes Bcl-2 protein, which is made up of 239 amino acids and it's molecular weight is 26Kb. The rearrangement of Bcl-2 gene is the result of chromosomal translocation t(14; 18). Both of the normal and translocation allele express a membrane-bound protein,locating in the mitochondrial membrane, blocking apoptosis. Livin is a new member of recently discovered new family of IAPs. It is one of the strongest inhibitors of apoptosis so far as found which mainly blocks the activation of death receptor and mitochondrial-based apoptosis channels through direct inhibition of factor caspase-3. Smac was first reported by Wang , which was isolated from HeLa cells. It is a new mitochondrial protein, and was named second mitochondrial-derived activator of caspase (Smac). It promoted apoptosis by the way of combining with IAPs,releasing caspase-9, 3, 7 from the inhibition of IAP, activating caspase cascade . Objective: The aim of this study was to work out the expression of Bcl-2, Livin and Smac in B-Cell NHL, the relationship between them and the relationship between the expression of them three and the clinical prognosis factors.Methods: The expression of Bcl-2, Livin and Smac was detected by way of immunohistochemical method in 40 specimens of B-cell NHL and 15 benign lymph node disorders .Results: The positive expression rates of Bcl-2 and Livin in B-cell NHL were 62.5%, 65%, respectively, the positive expression rates in benign lymph node disorders were26.7 %, 20 % . There are statistical significance between every two match (P<0.05). The positive expression rates of Smac in B-cell NHL was 60%, and that of benign lymph node was 80%. There is no statistical significance between them. (P>0.05)The expression of Bcl-2 and Livin in B-cell NHL had an obvious positive correlation (r=0.731, P<0.001). The expression of Bcl-2 and Smac in B-cell NHL had a negative correlation(r=-0.316, P<0.05). And the expression of Livin and Smac in B-cell NHL also showed a positive correlation(r=0.364, P<0.05). The positive expression level of Bcl-2, Livin had no relationship with the patients' sex, age, and Ann Arbor clinical stages(P>0.05). The positive expression level of Smac had no relationship with the patients' sex, age, (P>0.05), but was related with AnnArbor clinical stages(P<0.05).Conclusion: Bcl-2 and Livin in B-cell NHL may cooperate with each other to restrain cell apoptosis. Bcl-2 and Smac in B-cell NHL may resiste each other in the process of cell apoptosis. Livin and Smac may also cooperate with each other in the development of B-Cell NHL.