Two distinct types of cancer of different origin may be mixed in gastroesophageal junction adenocarcinomas in Japan: Evidence from direct evaluation of gastric acid secretion

Horii, Toru; Koike, Tomoyuki; Abe, Yasuhiko; Kikuchi, Ryosuke; Unakami, Hiroyuki; Iijima, Katsunori; Imatani, Akira; Ohara, Shuichi; Shimosegawa, Tooru

doi:10.3109/00365521.2011.565069

Cited by 28 publications

(32 citation statements)

References 42 publications

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“…In our study, the rate of H. pylori infection was significantly lower in patients with cardiac cancer than in patients with distal gastric cancer. Previous reports [24,45] support our results. Our study also revealed that the prevalence and degree of corporal gastritis were significantly lower in patients with GEJA than in patients with distal gastric cancer.…”

Section: Discussionsupporting

confidence: 83%

“…In addition, Horii et al [24] investigated the relationship between GEJA and gastric acid secretion using the endoscopic gastrin test. They demonstrated that 2 distinct types of cancer of different origin may be mixed in GEJA, including Barrett’s esophageal cancer, which is associated with high gastric acid secretion and reflux of gastric acid into the esophagus, and a cancer resembling distal gastric cancer associated with gastric atrophy and low gastric acid secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, both gastric acid and bile acid are important in the development of BE, which leads to Barrett’s esophageal cancer. Recent studies [22,23,24] showed that H. pylori infection is associated with significantly reduced risks of GEJA, but this was not observed for esophageal squamous cell carcinoma. The prevalence of GEJA, including Barrett’s esophageal cancer, may increase with an increase in BE occurrence and a reduction in the rate of H. pylori infection and H. pylori eradication in Japan [25].…”

Section: Introductionmentioning

confidence: 99%

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Relationship between Gastroesophageal Junction Adenocarcinoma and Helicobacter pylori Infection in Japan

Kamada

Kurose²,

Yamanaka³

et al. 2012

Digestion

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Background/Aims: The relationship between gastroesophageal junction adenocarcinoma (GEJA) and Helicobacter pylori infection is not well defined; thus, we retrospectively investigated this relationship. Methods: We examined 852 cases (646 men) of gastric cancer. GEJA was defined as type II according to the classification system of Siewert and Stein. We compared the prevalence of H. pylori infection and corporal gastritis in GEJA patients with distal gastric cancer. Results: GEJA was observed in 80 (including 6 cases of Barrett’s esophageal cancer) of the 852 cases of gastric cancer examined (9.4%). The rate of H. pylori infection was significantly lower in patients with GEJA than in patients with distal gastric cancer (73.8 vs. 94.1%, p < 0.05). The prevalence of corporal gastritis was also significantly lower in patients with GEJA than in patients with distal gastric cancer (80.7 vs. 94.6%, p < 0.05). Concurrent H. pylori infection and corporal gastritis were not observed in patients with Barrett’s esophageal cancer. Conclusion: Our study demonstrated that GEJA has 2 etiologic types; one of these types is associated with H. pylori infection and resembles distal gastric cancer, and the other one is not associated with H. pylori infection or Barrett’s esophageal cancer.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Relationship between Gastroesophageal Junction Adenocarcinoma and Helicobacter pylori Infection in Japan

Kamada

Kurose²,

Yamanaka³

et al. 2012

Digestion

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“…Intubation tests with direct measurement of acid secretion in patients with gastric cancer have only exceptionally been performed and a varying degree of impaired acid secretion has been reported in early gastric cancer [38]. However, atrophic gastritis is the most frequent precursor of gastric cancer and there is substantial indirect evidence of acid hyposecretion in intestinal-type gastric cancer by the determination of serum biomarkers [39,40,41,42].…”

Section: Acid Secretion and Gastric Cancermentioning

confidence: 99%

The Intriguing Relationship of Helicobacter pylori Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Malfertheiner

2011

Dig Dis

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Helicobacter pylori infection induces chronic inflammation of the gastric mucosa and thus profoundly affects gastric physiology. In the acute phase of infection, gastric acid secretion is transiently impaired. The morphological damage of the gastric mucosa, changes in gastric hormone release, and disruption of neural pathways all contribute to influence gastric acid secretion in a distinct manner. Changes in gastric acid secretion, whether impaired or increased, are intimately related with the topographic phenotypes of gastritis and the presence of atrophy or absence of corpus atrophy. The interplay of gastritis phenotype and acid secretion are key determinants in disease outcomes. Corpus-predominant gastritis and corpus atrophy are accompanied by hypochlorhydria and carry the highest risk for gastric cancer, whereas antrum-predominant gastritis with little involvement of the corpus-fundic mucosa is associated with hyperchlorhydria and predisposes to duodenal ulcer disease.

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“…The same group proposed that the preservation of gastric acid secretion might be important for the development of adenocarcinoma at the EGJ (including EAC) in Japanese people, irrespective of the H. pylori infection status [91]. Namely, there may be two distinct types of cancer at the EGJ-EAC (BE cancer) associated with high gastric acid secretion and reflux of gastric acid into the esophagus and EGJ adenocarcinoma (non-BE cancer) resembling distal gastric cancer associated with gastric atrophy and low gastric acid secretion [92,93].…”

Section: H Pylori Infection and Carcinogenesismentioning

confidence: 99%

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

Watari

Oshima

Fukui

et al. 2013

Clin J Gastroenterol

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Barrett's esophagus (BE) is a premalignant condition of esophageal adenocarcinoma (EAC). Although the incidence of BE has risen rapidly in the West, it is rare in Asia despite a recent increase in the prevalence of gastroesophageal reflux disease. Controversies over the definition of BE are presented because most cases show shortsegment BE, especially ultra-short BE, in Asia. Here we review possible risk factors for the development of EAC, particularly possible roles of ethnicity, specialized intestinal metaplasia (SIM), BE length, and environmental factors, such as Helicobacter pylori infection and obesity. Additionally, we summarize recent studies on the effect of chemoprevention including proton pump inhibitors, nonsteroidal anti-inflammatory drugs or aspirin in order to reduce the risk of neoplastic progression in BE patients. Although substantial knowledge of risk factors of dysplasia/EAC in BE is shown, the risk for neoplastic development may be influenced by geographic variation, study population, the presence or absence of SIM or dysplasia at baseline, and the small number of BE patients investigated. Recently, the efficiency of surveillance for BE patients has been discussed from the standpoint of cost-effectiveness. It may be too difficult to draw conclusions because no randomized clinical trials of BE surveillance have been performed.

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Two distinct types of cancer of different origin may be mixed in gastroesophageal junction adenocarcinomas in Japan: Evidence from direct evaluation of gastric acid secretion

Cited by 28 publications

References 42 publications

Relationship between Gastroesophageal Junction Adenocarcinoma and <i>Helicobacter pylori</i> Infection in Japan

Relationship between Gastroesophageal Junction Adenocarcinoma and <i>Helicobacter pylori</i> Infection in Japan

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

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