Literature DB >> 22186036

Gastric cancers emerging after H. pylori eradication arise exclusively from non-acid-secreting areas.

Katsunori Iijima1, Yasuhiko Abe, Tomoyuki Koike, Kaname Uno, Hiroyuki Endo, Waku Hatta, Naoki Asano, Kiyotaka Asanuma, Akira Imatani, Tooru Shimosegawa.   

Abstract

Although Helicobacter pylori (H. pylori) eradication has some inhibitory effects on the subsequent development of gastric cancer, there are sporadic cases of gastric cancer even after successful eradication. The pathogenesis of gastric cancer emerging after H. pylori eradication remains to be clarified. In this study, employing Congo-red chromoendoscopy, which is capable of visualizing the acid-secreting fundic mucosa, we investigated the topographic relationship of the acid secretion pattern to the occurrence site of gastric cancers emerging after eradication. Fourteen consecutive patients who suffered from new gastric cancer after eradication, defined as lesions that were discovered at least 2 years after the eradication, were prospectively enrolled. Whether the neoplasias arose from acid-secreting or non-acid-secreting areas was evaluated with Congo-red chromoendoscopy. Biopsy specimens taken from the two areas were subjected to histologic evaluation and immunohistochemistry for Ki-67 and p53. The mean period from the eradication to the subsequent occurrence of gastric cancer was 74 (44) months. There were two cancer lesions in 5 cases, and thus there was a total 19 lesions from 14 cases. Congo-red chromoendoscopy revealed that all 19 lesions arose exclusively from non-acid-secreting areas. Histological examination revealed sustained hyperproliferation and accumulation of p53 protein was frequently detectable in non-acid-secreting areas. Genetic alteration such as p53 mutation seems to be already present in the residual non-acid-secreting areas after eradication, areas that could be the origin of gastric carcinogenesis after eradication. Identification of such high-risk areas should be a promising approach for estimating the individual cancer risk after eradication.

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Year:  2012        PMID: 22186036     DOI: 10.1620/tjem.226.45

Source DB:  PubMed          Journal:  Tohoku J Exp Med        ISSN: 0040-8727            Impact factor:   1.848


  4 in total

Review 1.  Gastric cancer development after the successful eradication of Helicobacter pylori.

Authors:  Kaname Uno; Katsunori Iijima; Tooru Shimosegawa
Journal:  World J Gastrointest Oncol       Date:  2016-03-15

Review 2.  Alterations of the TP53 gene in gastric and esophageal carcinogenesis.

Authors:  Marilanda Ferreira Bellini; Aline Cristina Targa Cadamuro; Maysa Succi; Marcela Alcântara Proença; Ana Elizabete Silva
Journal:  J Biomed Biotechnol       Date:  2012-08-07

3.  Usefulness of Endoscopic Imaging to Visualize Regional Alterations in Acid Secretion of Noncancerous Gastric Mucosa after Helicobacter pylori Eradication.

Authors:  Kaname Uno; Katsunori Iijima; Yasuhiko Abe; Tomoyuki Koike; Yasushi Takahashi; Nobuyuki Ara; Tooru Shimosegawa
Journal:  J Gastric Cancer       Date:  2016-09-30       Impact factor: 3.720

Review 4.  Pathogenesis and risk factors for gastric cancer after Helicobacter pylori eradication.

Authors:  Reina Ohba; Katsunori Iijima
Journal:  World J Gastrointest Oncol       Date:  2016-09-15
  4 in total

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