Helicobacter pylori infection and oesophageal adenocarcinoma

In particular, Hp-I induced NF-κB and COX-2 expression in oesophageal epithelial cells, playing a role in inflammation associated with BO and tumorigenesis in the oesophagus [4]; upon colonizing oesophagus, Hp increases the severity of oesophageal inflammation and the incidence of BO and OAC [4]. [...]evidence indicates that: (a) Hp-I prevalence is high in BO; (b) neither Hp-I nor Hp-I by CagA+ strains reduce the risk of BO in certain populations with high prevalence of Hp-I; (c) the expected incidence of OAC with persistent Hp-I is higher than that of OAC after eradication of infection; Hp-I may affect specific molecular alterations (genetic instability, E-cadherin methylation, monoclonal antibody Das-1) associated with the pathogenesis of BO; and (d) Hp induces Ki-67 expression and increased oesophageal expression of Ki-67 observed in BO patients compared with GORD controls.