Role of Helicobacter pylori on differential expression of angiogenic markers in gastric adenocarcinoma

Document Type: Original Article


Animal studies showed that male gastric tissues respond more rapidly to Helicobacter pylori (H.pylori) infection but the possible mechanisms remained unclear. There is no data about gender specific activity of Androgen receptor (AR) as an independent unfavorable prognostic factor in gastric cancer and its interactions with H.pylori and angiogenesis in both genders. To compare the pathogenesis of H. pylori and to evaluate its role on tissue levels of Androgen Receptor (AR) and uPA as a major angiogenic factors in gastric adenocarcinoma, malignant and corresponding normal tissue specimens of 71 gastric adenocarcinoma were selected retrospectively. Modified Giemsa staining was used for identifying H.pylori infection and immunohistochemical methods were used to identify differential expressions of above markers in glandular, surface epithelial, tumoral, stromal, endothelial and lymphatic cells. Interestingly 83.3% of H.pylori positive males showed AR overexpression in their surface epithelial cells whereas the same interaction was not found in H.pylori positive females. Higher vascular invasion (p=0.047) and higher expression of uPA in stromal cells of male patients (p=0.007) clued us to different tumor progressive factors in males. Linear regression analysis showed H.pylori infection, surface epithelial AR and sex as three significant factors in tumoral uPA (p=0.004), stromal uPA (p=0.012) and lymphatic uPA (p=0.016) expression in males which play important roles on invasion and metastasis of gastric carcinoma. Present results suggest the strong role of H.Pylori on angiogenesis in males which could be considered as a new molecular mechanism of tumor progression by interacting with the receptor of male hormone and angiogenic pathways.