Association of PLUNC gene polymorphisms with susceptibility to nasopharyngeal carcinoma in a Chinese population

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Abstract
Genetic mapping of variants conferring a small disease risk can identify pathways in complex disorders. Thus, the hope of resolving the genetic aetiology of NPC and the mechanisms of racial and geographic differences in NPC susceptibility has prompted a search for genetic variants in gene candidates thought to play a role in the pathogenesis of the NPC. A genetic linkage study based on affected sibling pairs collected from different Chinese populations in southeast Asia, which located the susceptibility locus to within the 6p22 region, supported the involvement of the human leukocyte antigens (HLA) in the pathogenesis of NPC.11 Recently, two genomewide searches, carried out in 20 Cantonese speaking families from Guangdong province and 18 families from Hunan province in southern China, provided evidences of susceptibility loci for NPC on chromosome 4p15.1-q12 and 3p21.31–21.2, respectively.12,13 Case–control studies have established associations between specific HLA molecules and NPC in several populations including Asians, whites, and North Africans.14–16 In addition to the HLA, some non-HLA loci, including the heat shock protein 70-2 (HSP70-2),17 cyclin D1 (CCND1),18 glutathione S-transferase M1 (GSTM1),19 and CYP2E1 genes4 have also shown associations with susceptibility to NPC. Based on the fact that the disease susceptibility to NPC is determined at different functional levels, such as metabolism of carcinogenic constituents, tumour antigen presentation, cell cycle regulation, and antigenic peptide chaperones, we hypothesised that an unknown number of other unidentified genes are likely to modify the susceptibility to NPC.

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