The impact of Helicobacter pylori on EGF, EGF receptor, and the c-erb-B2 expression.
Authors:
Jurkowska, Grażyna Piotrowska-Staworko, Grażyna Guzińska-Ustymowicz, Katarzyna Kemona, Andrzej Świdnicka-Siergiejko, Agnieszka Łaszewicz, Wiktor Dąbrowski, Andrzej
Citation:
Jurkowska G, etal., Adv Med Sci. 2014 Sep;59(2):221-6. doi: 10.1016/j.advms.2014.01.006. Epub 2014 Jun 9.
PURPOSE: Increased expression of epidermal growth factor (EGF), its receptor (EGFR), and c-erb-B2 protein, which is homological with the EGF receptor, in gastric mucosa, may play a role in gastric carcinogenesis. We assessed if the infection and eradication of Helicobacter pylori (H. pylori) affects the gastric expression of growth factors and serum gastrin concentrations. PATIENTS/METHODS: We examined immunohistochemically gastric EGF and both receptors' expression in: gastric cancer (GC; n=29), chronic gastritis with H. pylori infection (GHp+; n=40) before and after eradication and in patients without H. pylori infection (GHp-; n=42). RESULTS: Before the eradication therapy, gastric mucosal EGF and both receptor's expressions in GHp+ patients were increased compared to GHp- (p<0.05), but were similar to GC. After eradication, EGF and the receptor's expression significantly decreased in the gastric body. Both EGFR and c-erb-B2 expression in the antrum were still higher than in GHp- (p<0.05), and remained comparable to GC. CONCLUSIONS: In patients with H. pylori infection the gastric mucosal EGF, EGFR, and c-erb-B2 expressions are similar to those observed in gastric cancer. The persistence of the antral expression of receptors after eradication, at a level comparable to the gastric cancer group, suggests their eventual role in the progression of changes initiated by H. pylori toward carcinogenesis.