Helicobacter pylori Eradication Prevents Extension of Intestinalization Even in the High-Risk Group for Gastric Cancer

Shiotani, Akiko; Nishi, Ryuji; Uedo, Noriya; Tsutsui, Hideaki; Ishii, Manabu; Imamura, Hiroshi; Kamada, Takenobu; Hata, Jiro; Haruma, Ken

doi:10.1159/000264651

Cited by 12 publications

(10 citation statements)

References 55 publications

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“…These findings are compatible with our previous data. Recently, Shiotani et al [24] reported that MUC2 expression decreased in the H. pylori -infected gastric mucosa with eradication therapy. This finding is apparently similar to our observations, though the cells examined were tumor, rather than non-neoplastic mucosal, cells.…”

Section: Discussionmentioning

confidence: 99%

Gastric Cancer Development after Helicobacter pylori Eradication Therapy: A New Form of Gastric Neoplasia

Matsuo¹,

Ito²,

Tatsugami³

et al. 2012

Digestion

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Background and Aim: Along with the widespread use of eradication for Helicobacter pylori (H. pylori), the incidence of gastric cancer after eradication has also been increasing. There is a need for clarification of the clinical and biological characteristics of these neoplasms. Patients and Methods: We studied 27 cases of gastric cancer that developed after eradication (group AE). Out of the 27, we selected 26 with early-stage gastric cancer and compared them with 78 age-matched gastric cancer patients with H. pylori infection (group Pos) and 20 patients without H. pylori (group Neg). The patient with autoimmune gastritis was not included. Clinicopathological features, mucus patterns and Wnt5a expressions were compared among these groups. Results: Among group AE patients, there were more males than females, and the tumor histology was mainly intestinal type, a significant difference from group Neg. In contrast, macroscopically, the tumors were predominantly of the flat-depressed type, a feature similar to that of group Neg but significantly different from that of group Pos. MUC2 and Wnt5a expression was significantly lower in group AE than in group Pos. Conclusion: Gastric cancer development after eradication may have a carcinogenic pathway similar to that in cancer with H. pylori infection, though macroscopic/biological features may be modified by eradication therapy.

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Section: Discussionmentioning

confidence: 99%

Gastric Cancer Development after Helicobacter pylori Eradication Therapy: A New Form of Gastric Neoplasia

Matsuo¹,

Ito²,

Tatsugami³

et al. 2012

Digestion

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“…GC develops through a cascade of well-defined stages (inflammation and atrophy, intestinal metaplasia, dysplasia, and carcinoma sequence) (Correa, 1988). The initial stages of gastritis and atrophy are attributed to infection by Helicobacter pylori (Hp) (Shiotani et al, 2010). Hp-related gastritis patients are at a high risk for developing GC, which may gradually progress to gastric intestinal metaplasia (Sipponen and Hyvärinen, 1993;Correa, 1995;Ohata et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA network analysis identifies key microRNAs and genes associated with precancerous lesions of gastric cancer

Wang¹,

Wu²,

Wang³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. To identify potential targets for the early treatment and prevention of gastric cancer, microRNA (miRNA) expression profiles of precancerous lesions of gastric cancer were investigated. The miRNA microarray dataset GSE24839 was downloaded from Gene Expression Omnibus (GEO) and included 10 Helicobacter pylori-related gastritis samples and 10 gastric intestinal metaplasia samples. Differentially expressed miRNAs (DEMs) were screened using the Student t-test; P < 0.05 was considered to be statistically significant. Co-expression networks of total miRNAs and DEMs were constructed based on the Pearson correlation coefficient for the two diseases. Target genes of the DEMs were retrieved using miRecords and pathway-enrichment analysis was performed using a hypergeometric test. A total of 20 DEMs were obtained for H. pylori-related gastritis and gastric intestinal metaplasia samples, including 12 up-regulated and 8 down-regulated miRNAs. The identified DEMs appear to play key roles in gastric cancer, as the average degree of the DEM sub-network was higher than that of the total miRNA co-expression network. Furthermore, target genes for 6 DEMs (hsa-miR-106b, hsa-miR-193a-3p, hsa-miR-204, hsa-miR-30e, hsa-miR-519d, and hsa-miR-524-5p) are in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, including signal transduction, cell growth and death, and transport and catabolism. Among the target genes, 5 (RAB22A, SOX4, IKZF2, PLAG1, and BTBD7) were of interest because they can be simultaneously regulated by several DEMs. These findings suggest that these genes may be targets for modulating gastric cancer progression.

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“…However, the point at which metaplastic changes make it difficult to detect whether endoscopic gastritis will completely regress after H. pylori eradication remains a matter of controversy. Although H. pylori eradication is known to reverse corpus atrophy and is the most effective method for reducing gastric cancer risk [2], the point in the disease at which H. pylori eradication fails to be effective remains to be established. Moreover, all histological IM (as evidenced by the presence of mucin-secreting goblet cells) in the stomach cannot be predicted using only endoscopic results, because of the variety of associated endoscopic features.…”

Section: Introductionmentioning

confidence: 99%

Endoscopic Diagnosis of Open-Type Atrophic Gastritis Is Related to the Histological Diagnosis of Intestinal Metaplasia and Cdx2 Expression

et al. 2011

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Unlike endoscopic diagnosis of closed-type atrophic gastritis, that of open-type atrophic gastritis is highly correlated with the histological diagnosis of IM and Cdx2 expression. Endoscopically diagnosed open-type atrophic gastritis and endoscopically diagnosed metaplastic gastritis have similar histological features, which suggests that a high percentage of IM cases are diagnosed as open-type atrophic gastritis by endoscopic examination.

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Helicobacter pylori Eradication Prevents Extension of Intestinalization Even in the High-Risk Group for Gastric Cancer

Cited by 12 publications

References 55 publications

Gastric Cancer Development after Helicobacter pylori Eradication Therapy: A New Form of Gastric Neoplasia

Gastric Cancer Development after Helicobacter pylori Eradication Therapy: A New Form of Gastric Neoplasia

MicroRNA network analysis identifies key microRNAs and genes associated with precancerous lesions of gastric cancer

Endoscopic Diagnosis of Open-Type Atrophic Gastritis Is Related to the Histological Diagnosis of Intestinal Metaplasia and Cdx2 Expression

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