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- W2110872517 abstract "The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread." @default.
- W2110872517 created "2016-06-24" @default.
- W2110872517 creator A5014254734 @default.
- W2110872517 creator A5020595493 @default.
- W2110872517 date "2006-07-06" @default.
- W2110872517 modified "2023-10-11" @default.
- W2110872517 title "Gastric angiogenesis and Helicobacter pylori infection" @default.
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- W2110872517 doi "https://doi.org/10.4321/s1130-01082006000700006" @default.
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