Gastric carcinogenesis: when is the point of no return?

Wright, N A

doi:10.1007/978-94-011-4882-5_35

Cited by 13 publications

(10 citation statements)

References 18 publications

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“…However, once dysplasia/cancer has developed in the background mucosa (Group DYS), both cellular phenotype, as detected by mAb Das-1 and neoplastic marker TC22, did not show significant change following H. pylori eradication. These data support the conclusion reported by some investigators that at a certain stage of progression of GIM there is a "Point of no return" (Wong et al, 2004;Wright, 1998). GIM is considered to be a pre-cancerous lesion of the stomach (Uemura et al, 2001;Wong et al, 2004), especially when it is incomplete or colonic type (type II & type III) metaplasia (Filipe & Jass, 1986;Mirza et al, 2003).…”

Section: Study 1 I N T H I S S T U D Y W E S H O W T H a T H Pylorsupporting

confidence: 86%

Effects of Helicobacter pylori Infection on the Histology, Cellular Phenotype, K-ras Mutations, and Cell Kinetics in Gastric Intestinal Metaplasia in Patients with Chronic Gastritis and Gastric Cancer

Watari¹,

Tanabe²,

Moriichi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

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Section: Study 1 I N T H I S S T U D Y W E S H O W T H a T H Pylorsupporting

confidence: 86%

Effects of Helicobacter pylori Infection on the Histology, Cellular Phenotype, K-ras Mutations, and Cell Kinetics in Gastric Intestinal Metaplasia in Patients with Chronic Gastritis and Gastric Cancer

Watari¹,

Tanabe²,

Moriichi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

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“…Based on our results, then, lesions that are newly or persistently positive for the markers including MSI or mAb Das‐1 after H. pylori eradication are at a certain stage of progression of IM, and may have passed the “point of no return,” a concept proposed by Wright44 and Wong et al 12. It remains possible, therefore, that these are patients who are at high risk of developing gastric cancer that may warrant more intensive endoscopic surveillance to detect early gastric cancer.…”

Section: Discussionmentioning

confidence: 73%

Biomarkers predicting development of metachronous gastric cancer after endoscopic resection: an analysis of molecular pathology of Helicobacter pylori eradication

Watari

Moriichi

Tanabe

et al. 2011

Intl Journal of Cancer

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Metachronous gastric cancer (MGC) after endoscopic resection (ER) of gastric cancer still occurs to some degree even after Helicobacter pylori (H. pylori) treatment. We evaluated whether two biomarkers related to carcinogenesis expressed in intestinal metaplasia (IM) become predictors for MGC development after eradication. We performed a hospital-based, case-control study of 75 patients, including 50 mucosal cancer patients who had undergone ER (Group DYS), and 25 age- and sex-matched chronic gastritis patients for whom H. pylori had been successfully eradicated (control). Additionally, Group DYS patients were divided into 2 groups: 25 successfully H. pylori-eradicated (eradicated group) and 25 un-eradicated patients (persistent group). All patients were followed for 1 year. We analyzed microsatellite instability (MSI) and immunoperoxidase assays using a monoclonal antibody for the colonic phenotype (Das-1). Both MSI and Das-1 reactivity in IM were significantly higher in Group DYS than in the control (p<0.05 and p<0.01, respectively). MSI and Das-1 reactivity were strong and independent predictors for gastric cancer (OR=7.09, 95% CI 1.27-39.6, p=0.03 for MSI and OR=4.96, 95% CI 1.64-15.0, p=0.005 for Das-1 reactivity). The incidence of MSI tended to decrease in the eradicated group (p=0.07), but not in the persistent group. The Das-1 immunoreactivity in IM also declined in both the eradicated group and the control. Interestingly, all MGCs after ER were positive for MSI or Das-1 reactivity. MSI or Das-1 reactivity in IM strongly predicts the development of MGC. Patients in whom these biomarkers persist after eradication may therefore have a high risk of developing MGC.

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“…Based on our results, then, lesions that are newly or persistently positive for the markers including MSI or mAb Das-1 after H. pylori eradication are at a certain stage of progression of IM, and may have passed the "point of no return" (Wong et al, 2004;Wright, 1998). It remains possible, therefore, that these are patients who are at high risk of developing gastric cancer that may warrant more intensive endoscopic surveillance to detect early gastric cancer.…”

Section: Discussionmentioning

confidence: 79%

Intestinal Metaplasia Related to Gastric Cancer: An Outcome Analysis of Biomarkers for Early Detection

Watari¹,

Moriichi²,

Tanabe³

et al. 2013

Current Topics in Gastritis - 2012

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Gastric carcinogenesis: when is the point of no return?

Cited by 13 publications

References 18 publications

Effects of Helicobacter pylori Infection on the Histology, Cellular Phenotype, K-ras Mutations, and Cell Kinetics in Gastric Intestinal Metaplasia in Patients with Chronic Gastritis and Gastric Cancer

Effects of Helicobacter pylori Infection on the Histology, Cellular Phenotype, K-ras Mutations, and Cell Kinetics in Gastric Intestinal Metaplasia in Patients with Chronic Gastritis and Gastric Cancer

Biomarkers predicting development of metachronous gastric cancer after endoscopic resection: an analysis of molecular pathology of Helicobacter pylori eradication

Intestinal Metaplasia Related to Gastric Cancer: An Outcome Analysis of Biomarkers for Early Detection

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