Mechanism of the Development of Esophagogastric Junction Adenocarcinoma Ken-ichi Mukaisho 1 , Takahisa Nakayama 1 , Yoshio Araki 1 , Tadashi Hagiwara 1 , Ryoji Kushima 2 , Takanori Hattori 1 , Hiroyuki Sugihara 1 1Department of Pathology, Division of Molecular Diagnostic Pathology, Shiga University of Medical Science, Otsu, Japan 2Department of Clinical Laboratory Medicine, Division of Diagnostic Pathology, Shiga University of Medical Science, Otsu, Japan Keyword: esophagogastric junction , adenocarcinoma , bile acid , Barrett's esophagus , Helicobacter pylori pp.1168-1175
Published Date 2015/8/25
DOI https://doi.org/10.11477/mf.1403200388
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 There are two distinct etiologies of cardia cancer subtypes, one of which is associated with gastroesophageal reflux. It predominantly occurs in patients without Helicobacter pylori(H. pylori)infection and resembles esophageal adenocarcinoma. Additionally, it can be developed in an environment of high volume reflux. N-nitroso compounds, generated at night in the gastric juice with the refluxate(including bile acids), and a highly acidic condition also contribute to carcinogenesis by acting as a stabilizer of N-nitroso bile acids. The other etiology is associated with H. pylori atrophic gastritis and resembles noncardia cancer. It can be associated with the changing colonization of H. pylori from the distal to the proximal stomach with atrophic gastritis caused by a high concentration of soluble bile acids in an environment of low acid production. Under these conditions, soluble bile acids are likely to act as a bactericide or chemorepellent for H. pylori in the distal stomach. In this manuscript, we describe the potential mechanisms involved in the development of gastric cardia adenocarcinoma by elucidating the interactions among pH, H. pylori, and bile acids.

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