The aim of the study was to evaluate the role of Helicobacter pylori CagA(+) infection in gastric cancer.
475 patients were included into the study (270 gastric cancer patients and 205 control subjects). Helicobacter pylori CagA status was determined by enzyme-linked immunoabsorbent assay (ELISA). The frequency of H. pylori CagA infection in gastric cancer patients and control group was compared. The relationship between presence of anti-H. pylori CagA antibodies and selected clinical and pathomorphological parameters was analysed.
Gastric cancer patients and controls had the same prevalence of H. pylori CagA antibodies (54.4 vs 52.5%; p = 0.078). The persons with H. pylori CagA(+) and CagA(-) were at the same risk for developing gastric cancer (OR = 1.08; 95%CI = 0.66-1.49). However subgroup analysis showed that the risk of gastric cancer development in H. pylori CagA(+) depended on age being 2 times higher for young people (15-40 years) (OR = 2.0; 95% CI = 0-4.25) and four times higher for those under the age of 30 years (OR = 4.0; 95%CI = 0-15.9). There was a positive relationship between H. pylori CagA(+) infection and age (p = 0.043). H. pylori CagA(+) infection was independent of sex, family history of cancers, duration of symptoms, ABO blood group, tumour site, stage, histology and p53 accumulation in cancer gastric tissue.
Our study shows that H. pylori CagA(+) infection increases the risk for developing gastric cancer in young persons and does not protect the host against cardia cancer. The results suggest also that infection by H. pylori CagA(+) in gastric cancer has no influence on p53 gene mutation development.