No Association of MUC1 Gene Polymorphisms with H. pylori Infection and Non-cardia Gastric Cancer Risk in Chinese

Gastric cancer, the second most common cause of cancer-related death in the world, is characterized as a multifactorial disease that results from individual genetic predisposition and exposure to environmental factors (Brenner et al., 2009). According to anatomic site, gastric cancer can be classified as cardia and non-cardia subtypes. In non-cardia gastric cancer, Helicobacter pylori (H. pylori) infection is an established etiological factor (Peek and Blaser, 2002). However, nearly half of the world’s population is infected with H. pylori, but only a very small proportion of those infected eventually develop noncardia gastric cancer (Peek and Blaser, 2002), suggesting that genetic factors of host may play an important role in gastric carcinogenesis. Upon infection, H. pylori primarily resides within the mucus layer, adhering to mucins, high molecular weight glycoproteins and major components of the protective layer across the upper mucous surfaces (Peek and Blaser, 2002; Lindén et al., 2008). Some works have documented the role of MUC1 in the H. pylori infection and gastric cancer risk. Thus, MUC1 is often aberrantly expressed in stomach cancer, and it is a ligand for H. pylori (Ng et al., 2008). Susceptibility to H. pylori infection and gastric cancer appears to be associated with MUC1 allele length (Costa et al., 2008; Vinall et al., 2002). Recently,