Usefulness of gastric cancer screening using the serum pepsinogen test method

Morita, Masuo; Sasajima, Masahiko; Hoshina, Reiko; Kanda, Eiko; Urita, Yoshihisa

doi:10.1111/j.1572-0241.2003.07410.x

Cited by 180 publications

(117 citation statements)

References 17 publications

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“…Using these values, sensitivity and specificity of screening for gastric cancer are reported to be 80% and 70%, respectively, and the cancer detection rate is 0.44%. 30 However, in our present study, using that cut-off, the sensitivity and specificity were only 77% and 52%, respectively, possibly related to the fact that our agematched control subjects were older than the screened populations in previous studies. In our study, the combination of PG I concentration of 45 ng/mL or less and gastrin 17 of more than 60 pg/mL was the most suitable marker.…”

Section: Discussioncontrasting

confidence: 77%

Histologic and serum risk markers for noncardia early gastric cancer

Shiotani

Uedo

Kumamoto³

et al. 2005

Intl Journal of Cancer

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Corpus dominant gastritis and intestinal metaplasia (IM) are considered markers of increased risk of gastric carcinoma. The aim of our study was to determine serum and histologic risk markers of gastric cancer. Antral and corpus histology, pepsinogen and gastrin 17 levels were compared among patients with history of endoscopic mucosal resection (EMR) for early gastric cancer and controls. Serum pepsinogen (PG) and gastrin 17 levels were measured by RIA. There were 53 gastric cancer patients and 75 controls. The scores for IM in each region and atrophy at the lesser curvature of the corpus were significantly higher in the cancer group than in the H. pylori-positive control group. IM at the greater curvature of the corpus and atrophy at the lesser curvature of the corpus were associated with multiple malignant lesions. Although corpus gastritis was associated with an increased risk of gastric cancer (odds ratio [OR] = 3.4; 95% confidence interval [CI] 1.6-7.0) (p = 0.001), the most important marker was the presence of IM at the lesser curvature of the corpus (OR = 15.1; 95% CI 4.3-52.6) (p < 0.001)). The best cut-off points of serum markers for gastric cancer were a PG I concentration of 45 ng/mL or less and a gastrin 17 >60 pg/mL (sensitivity = 83%; specificity = 68%). IM at the lesser curvature of the corpus and the combination of serum gastrin 17 and PG I identified a group at high risk for development of gastric cancer. Annual endoscopic follow-up is warranted for patients with IM found at the greater curvature of the corpus. ' 2005 Wiley-Liss, Inc.

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Section: Discussioncontrasting

confidence: 77%

Histologic and serum risk markers for noncardia early gastric cancer

Shiotani

Uedo

Kumamoto³

et al. 2005

Intl Journal of Cancer

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“…thus, a full understanding of the molecular mechanism of carcinogenesis and identification of biomarkers for the early diagnosis and effective treatment of human GC are crucial. Although several serum biomarkers have been researched as new invasive tools for screening GC (6)(7)(8)(9), these serum tests are not available as screening or surveillance tests due to their low specificity and sensitivity (9). Biomarkers derived from tumor tissues may provide higher sensitivity and specificity than those from serum (10), yet tissue specimens must be obtained by invasive means involving endoscopy and biopsy.…”

Section: Introductionmentioning

confidence: 99%

Tissue metabolomic fingerprinting reveals metabolic disorders associated with human gastric cancer morbidity

Wang²,

Liu³

et al. 2011

Oncol Rep

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Abstract. the principal way to improve the outcome of gastric cancer (GC) is to predict carcinogenesis and metastasis at an early stage. the aims of the present study were to test the hypothesis that distinct metabolic profiles are reflected in GC tissues and to further explore potential biomarkers for GC diagnosis. Gas chromatography/mass spectrometry (GC/Ms) was utilized to analyze tissue metabolites from 30 GC patients. A diagnostic model for GC was constructed using orthogonal partial least squares discriminant analysis (OpLs-DA), and the metabolomic data were analyzed using the non-parametric Wilcoxon rank sum test to identify the metabolic tissue biomarkers for GC. Over 100 signals were routinely detected in one single total ion current (tIC) chromatogram, and the OPLS-DA model generated from the metabolic profile of the tissues adequately discriminated the GC tissues from the normal mucosae. Among the low-molecular-weight endogenous metabolites, a total of 41 compounds, such as amino acids, organic acids, carbohydrates, fatty acids and steroids, were detected, and 15 differential metabolites were identified with significant difference (p<0.05). A total of 20 variables were noted which contributed to a great extent in the discriminating OpLs-DA model (VIp value >1.0), among which 12 metabolites were identified using both VIP values (VIP >1) and the Wilcoxon test (p<0.05). In conclusion, the identification of the metabolites associated with GC morbidity potentially revealed perturbations of glycolysis, fatty acid β-oxidation, cholesterol and amino acid metabolism. these results suggest that tissue metabolic profiles have great potential in detecting GC and may aid in understanding its underlying mechanisms.

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“…its evaluation based on serum pepsinogen tests is a useful means of assessing cancer risk (12,20). To evaluate the relationship between RASGRF1 methylation and mucosal atrophy, we divided the samples based on the pepsinogen test results and then generated respective ROC curves.…”

Section: Analysis Of Rasgrf1 Methylation and Expression In Gastric Camentioning

confidence: 99%

Aberrant Methylation of RASGRF1 Is Associated with an Epigenetic Field Defect and Increased Risk of Gastric Cancer

Takamaru

Yamamoto

Suzuki

et al. 2012

Cancer Prevention Research

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Aberrant DNA methylation is implicated in the epigenetic field defect seen in gastric cancer. Our aim in this study was to identify predictive biomarkers by screening for DNA methylation in noncancerous background gastric mucosa from patients with gastric cancer. Using methylated-CpG island amplification coupled with CpG island microarray (MCAM) analysis, we identified 224 genes that were methylated in the noncancerous gastric mucosa of patients with gastric cancer. Among them, RASGRF1 methylation was significantly elevated in gastric mucosa from patients with either intestinal or diffuse type gastric cancer, as compared with mucosa from healthy individuals (8.3% vs. 22.4%, P < 0.001; 8.3% vs. 19.4%, P < 0.001). RASGRF1 methylation was independent of mucosal atrophy and could be used to distinguish both serum pepsinogen test-positive [sensitivity, 70.0%; specificity, 86.7%; area under the receiver operator characteristic (ROC) curve, AUC, 0.763] and -negative patients with gastric cancer (sensitivity, 72.2%; specificity, 87.0%; AUC, 0.844) from healthy individuals. Ectopic expression of RASGRF1 suppressed colony formation and Matrigel invasion by gastric cancer cells, suggesting it may be involved in gastric tumorigenesis. Collectively, our data suggest that RASGRF1 methylation is significantly involved in an epigenetic field defect in the stomach, and that it could be a useful biomarker to identify individuals at high risk for gastric cancer. Cancer Prev Res; 5(10); 1203-12. Ó2012 AACR.

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Usefulness of gastric cancer screening using the serum pepsinogen test method

Abstract: The pepsinogen test method can be used as a screening test for high-risk subjects with atrophic gastritis, rather than as a tool for cancer itself. Systemic endoscopic surveillance of this group is also useful.

Cited by 180 publications

References 17 publications

Histologic and serum risk markers for noncardia early gastric cancer

Histologic and serum risk markers for noncardia early gastric cancer

Tissue metabolomic fingerprinting reveals metabolic disorders associated with human gastric cancer morbidity

Aberrant Methylation of RASGRF1 Is Associated with an Epigenetic Field Defect and Increased Risk of Gastric Cancer

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