Effects of Helicobacter pylori eradication on the development of metachronous gastric cancer after endoscopic treatment: analysis of molecular alterations by ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12-15

AUTHORS

Maki Kawanaka, Jiro Watari, Noriko Kamiya, Takahisa Yamasaki, Takashi Kondo, Fumihiko Toyoshima, Hisatomo Ikehara, Toshihiko Tomita, Tadayuki Oshima, Hirokazu Fukui, Takashi Daimon, Kiron M Das, Hiroto Miwa

ABSTRACT

Background:Whether Helicobacter pylori eradication actually suppresses the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) remains controversial. The aims of this study were to clarify (1) the molecular markers related to carcinogenesis in intestinal metaplasia (IM) by a cross-sectional study, and (2) the changes of those markers by an open-label, randomised controlled trial (RCT) of H. pylori treatment.Methods:First, we evaluated microsatellite instability (MSI), the methylation status at hMLH1, CDKN2A and APC genes, and immunoreactivity using the monoclonal antibody (mAb) Das-1 in IM in the background mucosa of 131 patients who underwent ER for gastric neoplasia and 22 chronic gastritis cases (control). Next, we performed an RCT to evaluate the changes of MSI between the H. pylori-eradicated (n=19) and non-eradicated patients (n=17) at 1 year among the H. pylori-positive patients.Results:Microsatellite instability and mAb Das-1 reactivity showed significantly higher incidences in both the H. pylori-positive and -negative patients compared with the control group, thus suggesting that MSI and mAb Das-1 reactivity are associated with gastric neoplasia (OR=5.06 for MSI; OR=2.51 for mAb Das-1 reactivity). The RCT showed that H. pylori eradication did not provide significant reversals of any molecular alterations including MSI (the primary end point) and other methylation statuses and mAb Das-1 reactivity (secondary end points).Conclusions:H. pylori eradication did not produce significant changes in the molecular alterations related to carcinogenesis, suggesting that H. pylori treatment may not prevent the development of MGC in background mucosa with IM. More... »

PAGES

21-29

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/bjc.2015.418

DOI

http://dx.doi.org/10.1038/bjc.2015.418

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021770280

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26671747


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29 schema:description Background:Whether Helicobacter pylori eradication actually suppresses the development of metachronous gastric cancer (MGC) after endoscopic resection (ER) remains controversial. The aims of this study were to clarify (1) the molecular markers related to carcinogenesis in intestinal metaplasia (IM) by a cross-sectional study, and (2) the changes of those markers by an open-label, randomised controlled trial (RCT) of H. pylori treatment.Methods:First, we evaluated microsatellite instability (MSI), the methylation status at hMLH1, CDKN2A and APC genes, and immunoreactivity using the monoclonal antibody (mAb) Das-1 in IM in the background mucosa of 131 patients who underwent ER for gastric neoplasia and 22 chronic gastritis cases (control). Next, we performed an RCT to evaluate the changes of MSI between the H. pylori-eradicated (n=19) and non-eradicated patients (n=17) at 1 year among the H. pylori-positive patients.Results:Microsatellite instability and mAb Das-1 reactivity showed significantly higher incidences in both the H. pylori-positive and -negative patients compared with the control group, thus suggesting that MSI and mAb Das-1 reactivity are associated with gastric neoplasia (OR=5.06 for MSI; OR=2.51 for mAb Das-1 reactivity). The RCT showed that H. pylori eradication did not provide significant reversals of any molecular alterations including MSI (the primary end point) and other methylation statuses and mAb Das-1 reactivity (secondary end points).Conclusions:H. pylori eradication did not produce significant changes in the molecular alterations related to carcinogenesis, suggesting that H. pylori treatment may not prevent the development of MGC in background mucosa with IM.
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35 schema:keywords APC gene
36 CDKN2A
37 DA-1
38 Das-1 reactivity
39 H. pylori eradication
40 H. pylori treatment
41 H. pylori-positive patients
42 Helicobacter pylori eradication
43 RCTs
44 aim
45 alterations
46 analysis
47 background mucosa
48 cancer
49 carcinogenesis
50 cases
51 changes
52 chronic gastritis cases
53 control group
54 cross-sectional study
55 development
56 development of MGC
57 effect
58 endoscopic resection
59 endoscopic treatment
60 eradication
61 gastric cancer
62 gastric neoplasia
63 gastritis cases
64 genes
65 group
66 hMLH1
67 high incidence
68 immunoreactivity
69 incidence
70 instability
71 intestinal metaplasia
72 markers
73 metachronous gastric cancer
74 metaplasia
75 methylation status
76 microsatellite instability
77 molecular alterations
78 molecular markers
79 monoclonal antibody Das-1
80 mucosa
81 negative patients
82 neoplasia
83 non-eradicated patients
84 patients
85 pylori eradication
86 pylori treatment
87 pylori-positive patients
88 reactivity
89 resection
90 reversal
91 significant changes
92 significant reversal
93 status
94 study
95 treatment
96 trials
97 years
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