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Abstract Tumors are generally classified as either liquid or solid. The former includes leukemia and lymphoma comprising neoplastic cells whose precursors are usually motile. Solid tumors comprise either epithelial or mesenchymal cells that are usually immobile. Lymphoma, which originates in the cells of the immune system include HL and NHL (Pelengaris and Khan, 2006). NHL is the sixth most common cause of cancer death; representing 4% of all cancer cases (Horikawa et al., 2011; McNally, 2011). Approximately 287,000 new cases of NHL were annually reported (Oluwasola et al., 2011). In Egypt, lymphoma is the most common cancer in children and NHL is the second most common cancer in adults (Soliman and Boffetta, 2006). Cytokines are secreted proteins that play a critical role in regulating the immune system; they control lymphoid cell development and differentiation, and regulate the balance between the Th1 and Th2, immune responses. Given these biologic properties, there is reason to postulate that cytokine activity might influence the pathogenesis of NHL (Purdue et al., 2007). Many cytokines are known to be involved in the pathogenesis of NHLs including IL-10 and IL-6 which act as a growth factor for normal activated human B and T lymphocyte stimulation and proliferation (El-Far et al., 2004; Skibola et al., 2007). Some studies focused on the role of both cytokines in NHL following CD38 expression. A secretion of IL-6 and IL-10 upon CD38 ligation has been demonstrated in the study of Malavasi et al. (2008). Furthermore, Xu et al. (2004) found that IL-10 augmented the expression of CD38 on plasma cells. A number of studies have examined the role of genetic polymorphisms in the development of malignant lymphomas. Various genes have been evaluated, including 144 genes that: influence DNA integrity and methylation; involved in xenobiotic metabolism; involved in innate immunity, oxidative stress, energy regulation and hormone production; and, that alter B-cell survival and growth, such as those of proinflammatory and regulatory cytokines (Hennessy et al., 2004). |