**2.2.3 Genetic factors and family history**

Family history and genetic factors increase risk of NHL in people whose relatives previously were diagnosed with NHL, but hereditary factors are hypothesized to account only for a small percentage of NHL and are unlikely to explain the increase in NHL incidence. Tumor suppressor genes, oncogenes and DNA repair genes may play a role in NHL carcinogenesis, and some genes may interact with environmental exposures that affect NHL risk (Fisher & Fisher, 2004). In a US multicenter case–control study, Chatterjee *et. al* showed *(Chatterjee, et al., 2004)* the strongest associations were found among siblings (HR = 7.6, 95% CI: 0.98–58.8) and male relatives (HR = 6.2, 95% CI: 0.77–50.0) of NHL cases. For a parental history of histopathologically concordant lymphoma, the strongest associations with lymphoma risk among offspring were found for B-cell lymphoma (SIR = 11.8, 95% CI: 2.2–34.8) and follicular lymphoma (SIR = 6.1, 95% CI: 1.1–18.0) *(Altieri, Bermejo, & Hemminki, 2005).*

Several genetic polymorphisms associated with the risk of NHL suggest that single nucleotide polymorphisms (SNPs) in tumor necrosis factor (TNF) and interleukin-10 (IL10) are associated with risk of NHL, especially diffuse large B –cell lymphoma. Relatively few studies have examined the potential interaction between germline susceptibility and environmental or lifestyle factors in the etiology of NHL (Alexander, et al., 2007). The mechanism (s) by which genetic predisposition or gene-environment interactions may enhance or reduce the risk of developing NHL remains a largely unexplored area of research (Alexander, et al., 2007).
