Relationship between Gastroesophageal Junction Adenocarcinoma and &lt;i&gt;Helicobacter pylori&lt;/i&gt; Infection in Japan

Kamada, Takenobu; Kurose, Hiromichi; Yamanaka, Yoshiaki; Manabe, Noriaki; Kusunoki, Hiroaki; Shiotani, Akiko; Inoue, Kentaro; Hata, Jiro; Matsumoto, Hideo; Akiyoshi, Takashi; Hirai, Toshihiro; Sadahira, Yoshito; Haruma, Ken

doi:10.1159/000336352

Cited by 25 publications

(15 citation statements)

References 74 publications

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“…While early studies claim that H. pylori infection is only related to distal or ‘non-cardia' gastric cancer, this is no longer true since there is clear evidence now for the pathogenetic relevance also in proximal gastric cancer or adenocarcinomas at the esophagogastric junction, if proper allocation of the tumor and assessment of the relevant risk factor are performed [15,16,17]. The risk for gastric carcinogenesis by H. pylori infection is similar for intestinal- and diffuse-type gastric cancers [15,18].…”

Section: Helicobacter Pylori - Epidemiological Backgroundmentioning

confidence: 99%

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

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Infection with Helicobacter pylori is established as the major risk factor for gastric cancer development. Damage of the mucosal barrier due to H. pylori-induced inflammation enhances the carcinogenic effect of other risk factors such as salt intake or tobacco smoking. The genetic disposition of both the bacterial strain and the host can increase the potential towards gastric cancer formation. Genetic variance of the bacterial proteins CagA and VacA is associated with a higher gastric cancer risk, as are polymorphisms and epigenetic changes in host gene coding for interleukins (IL1β, IL8), transcription factors (CDX2, RUNX3) and DNA repair enzymes. Application of high-throughput assays for genome-wide assessment of either genetic structural variance or gene expression patterns may lead to a better understanding of the pathobiological background of these processes, including the underlying signaling pathways. Understanding of the stepwise alterations that take place in the transition from chronic atrophic gastritis, via metaplastic changes, to invasive neoplasia is vital to define the ‘point of no return' before which eradication of H. pylori has the potential to prevent gastric cancer. Currently, eradication as preventive strategy is only recommended for high-incidence regions in Asia; large population studies with an adequate follow-up are required to demonstrate the effectiveness of such an approach in Western populations.

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Section: Helicobacter Pylori - Epidemiological Backgroundmentioning

confidence: 99%

Helicobacter pylori and Gastric Cancer

Bornschein

Malfertheiner

2014

Dig Dis

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“…Some miRNAs have been shown to possess oncogenic or tumour suppressor activity and relate to apoptosis, proliferation, differentiation, metastasis, angiogenesis and immune response, which are all potentially involved in cancer initiation, progression and treatment response (Lu et al , 2005; Wang et al , 2010). There have been an increasing number of studies showing overexpression or downregulation of specific miRNAs in various malignant tumours including gastric cancer and H. pylori -infected gastric mucosa (Okubo et al , 2010; Hishida et al , 2011; Kamada et al , 2012; Shiotani et al , 2012a). …”

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confidence: 99%

Identification of serum miRNAs as novel non-invasive biomarkers for detection of high risk for early gastric cancer

et al. 2013

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Background:Many micro-RNAs (miRNAs) are differentially expressed in Helicobacter pylori-infected gastric mucosa and in gastric cancer tissue and previous reports have suggested the possibility of serum miRNAs as complementary tumour markers. The aim of the study was to investigate serum miRNAs and pepsinogen levels in individuals at high risk for gastric cancer both before and after H. pylori eradication.Methods:Patients with recent history of endoscopic resection for early gastric cancer and the sex- and age-matched controls were enrolled. Serum was collected from subjects before or after eradication and total RNA was extracted to analyse serum levels of 24 miRNAs. Serum pepsinogen (PG) I and II levels were measured using enzyme-linked immunosorbent assay kits.Results:Using miR-16 as an endogenous control, the relative levels of miR-106 and let-7d before and after H. pylori eradication and miR-21 after eradication were significantly higher in the high-risk group than in the controls. H. pylori eradication significantly decreased miR-106b levels and increased let-7d only in the control group. After eradication, the combination MiR-106b with miR-21 was superior to serum pepsinogen and the most valuable biomarker for the differentiating high-risk group from controls.Conclusion:Serum miR-106b and miR-21 may provide a novel and stable marker of increased risk for early gastric cancer after H. pylori eradication.

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“…69 Meanwhile, Derakhshan et al suggested that cardia cancer had two distinct etiologies: one arising from chronic gastritis similar to non-cardia cancer, and the other related to GERD similar to esophageal adenocarcinoma 21 and this was confirmed later in a study by Horii et al 22 In Western countries, most EGJ adenocarcinomas have characteristics similar to those of esophageal adenocarcinomas, in contrast to Asian countries where most have characteristics similar to those of distal gastric cancers. 22,70 The reason for the above difference between the West and East may be the more frequent incidence of H. pylori-related gastric cancers and ethnicity factors in the East. The variable prevalence of GERD, obesity, and H. pylori infection, and the pattern of gastric atrophy (corpus-or antrum-predominant) may explain the observed differences in incidence and time trends between the three Asian countries.…”

Section: Surgical Treatmentmentioning

confidence: 99%

Different time trend and management of esophagogastric junction adenocarcinoma in three Asian countries

Hatta

Tong

Lee

et al. 2017

Digestive Endoscopy

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Esophagogastric junction (EGJ) adenocarcinoma has been on the increase in Western countries. However, in Asian countries, data on the incidence of EGJ adenocarcinoma are evidently lacking. In the present review, we focus on the current clinical situation of EGJ adenocarcinoma in three Asian countries: Japan, Hong Kong, and Malaysia. The incidence of EGJ adenocarcinoma has been reported to be gradually increasing in Malaysia and Japan, whereas it has stabilized in Hong Kong. However, the number of cases in these countries is comparatively low compared with Western countries. A reason for the reported difference in the incidence and time trend of EGJ adenocarcinoma among the three countries may be explained by two distinct etiologies: one arising from chronic gastritis similar to distal gastric cancer, and the other related to gastroesophageal reflux disease similar to esophageal adenocarcinoma including Barrett's adenocarcinoma. This review also shows that there are several concerns in clinical practice for EGJ adenocarcinoma. In Hong Kong and Malaysia, many EGJ adenocarcinomas have been detected at a stage not amenable to endoscopic resection. In Japan, histological curability criteria for endoscopic resection cases have not been established. We suggest that an international collaborative study using the same definition of EGJ adenocarcinoma may be helpful not only for clarifying the characteristics of these cancers but also for improving the clinical outcome of these patients.

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

Cited by 25 publications

References 74 publications

Helicobacter pylori and Gastric Cancer

Helicobacter pylori and Gastric Cancer

Identification of serum miRNAs as novel non-invasive biomarkers for detection of high risk for early gastric cancer

Different time trend and management of esophagogastric junction adenocarcinoma in three Asian countries

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