For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
58
views
52
references
 Top references
cited by
100
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      292
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Gastric cancer screening by combined assay for serum anti- Helicobacter pylori IgG antibody and serum pepsinogen levels — “ABC method”

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The current status of screening for gastric cancer-risk (gastritis A, B, C, D) method using combined assay for serum anti- Helicobacter pylori ( Hp) IgG antibody and serum pepsinogen (PG) levels, “ABC method”, was reviewed and the latest results of our ongoing trial are reported. It was performed using the following strategy: Subjects were classified into 1 of 4 risk groups based on the results of the two serologic tests, anti- Hp IgG antibody titers and the PG I and II levels: Group A [ Hp(−)PG(−)], infection-free subjects; Group B [ Hp(+)PG(−)], chronic atrophic gastritis (CAG) free or mild; Group C [ Hp(+)PG(+)], CAG; Group D [ Hp(−)PG(+)]), severe CAG with extensive intestinal metaplasia. Continuous endoscopic follow-up examinations are required to detect early stages of gastric cancer. Asymptomatic Group A, which accounts for 50–80% of all the subjects may be excluded from the secondary endoscopic examination, from the viewpoint of efficiency. Hp-infected subjects should be administered eradication treatment aimed at the prevention of gastric cancer.

          Related collections

          Most cited references52

          • Record: found
          • Abstract: found
          • Article: not found

          Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer: an open-label, randomised controlled trial.

          Kazutoshi Fukase, Mototsugu Kato, Shogo Kikuchi … (2008)
          The relation between Helicobacter pylori infection and gastric cancer has been proven in epidemiological studies and animal experiments. Our aim was to investigate the prophylactic effect of H pylori eradication on the development of metachronous gastric carcinoma after endoscopic resection for early gastric cancer. In this multi-centre, open-label, randomised controlled trial, 544 patients with early gastric cancer, either newly diagnosed and planning to have endoscopic treatment or in post-resection follow-up after endoscopic treatment, were randomly assigned to receive an H pylori eradication regimen (n=272) or control (n=272). Randomisation was done by a computer-generated randomisation list and was stratified by whether the patient was newly diagnosed or post-resection. Patients in the eradication group received lansoprazole 30 mg twice daily, amoxicillin 750 mg twice daily, and clarithromycin 200 mg twice daily for a week; those in the control group received standard care, but no treatment for H pylori. Patients were examined endoscopically at 6, 12, 24, and 36 months after allocation. The primary endpoint was diagnosis of new carcinoma at another site in the stomach. Analyses were by intention to treat. This trial is registered with the UMIN Clinical Trials Registry, number UMIN000001169. At 3-year follow-up, metachronous gastric carcinoma had developed in nine patients in the eradication group and 24 in the control group. In the full intention-to-treat population, including all patients irrespective of length of follow-up (272 patients in each group), the odds ratio for metachronous gastric carcinoma was 0.353 (95% CI 0.161-0.775; p=0.009); in the modified intention-to-treat population, including patients with at least one post-randomisation assessment of tumour status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.339 (95% CI 0.157-0.729; p=0.003). In the eradication group, 19 (7%) patients had diarrhoea and 32 (12%) had soft stools. Prophylactic eradication of H pylori after endoscopic resection of early gastric cancer should be used to prevent the development of metachronous gastric carcinoma. Hiroshima Cancer Seminar Foundation.
          Article 0 comments Cited 336 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Oncogenic mechanisms of the Helicobacter pylori CagA protein.

            Masanori Hatakeyama (2004)
            Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies have shed light on the mechanism through which the cagA gene product, CagA, elicits pathophysiological actions. CagA is delivered into gastric epithelial cells by the bacterial type IV secretion system, where it deregulates the SHP2 oncoprotein. Intriguingly, CagA is noted for its variation, particularly at the SHP2-binding site, which could affect the potential of different strains of H. pylori to promote gastric carcinogenesis.
            Article 0 comments Cited 219 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Predicting the development of gastric cancer from combining Helicobacter pylori antibodies and serum pepsinogen status: a prospective endoscopic cohort study.

              T Mitsushima, H Doi, Y. Yamaji … (2005)
              Helicobacter pylori infection and gastric atrophy are both risk factors for gastric cancer. We aimed to elucidate the natural history of gastric cancer development according to H pylori infection and gastric atrophy status. A total of 9293 participants in a mass health appraisal programme were candidates for inclusion in the present prospective cohort study: 6983 subjects revisited the follow up programme. Subjects were classified into four groups according to serological status at initial endoscopy. Group A (n = 3324) had "normal" pepsinogen and were negative for H pylori antibody; group B (n = 2134) had "normal" pepsinogen and were positive for H pylori antibody; group C (n = 1082) had "atrophic" pepsinogen and were positive for H pylori antibody; and group D (n = 443) had "atrophic" pepsinogen and were negative for H pylori antibody. Incidence of gastric cancer was determined by annual endoscopic examination. Mean duration of follow up was 4.7 years and the average number of endoscopic examinations was 5.1. The annual incidence of gastric cancer was 0.04% (95% confidence interval (CI) 0.02-0.09), 0.06% (0.03-0.13), 0.35% (0.23-0.57), and 0.60% (0.34-1.05) in groups A, B, C, and D, respectively. Hazard ratios compared with group A were 1.1 (95% CI 0.4-3.4), 6.0 (2.4-14.5), and 8.2 (3.2-21.5) in groups B, C, and D, respectively. Age, sex, and "group" significantly served as independent valuables by multivariate analysis. The combination of serum pepsinogen and anti-H pylori antibody provides a good predictive marker for the development of gastric cancer.
              Article 0 comments Cited 100 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Proc Jpn Acad Ser B Phys Biol Sci
                Journal ID (publisher-id): PJAB
                Title: Proceedings of the Japan Academy. Series B, Physical and Biological Sciences
                Publisher: The Japan Academy (Tokyo, Japan )
                ISSN (Print): 0386-2208
                ISSN (Electronic): 1349-2896
                Publication date (Print): 25 July 2011
                Volume: 87
                Issue: 7
                Pages: 405-414
                Affiliations
                [*1 ]Japan Research Foundation of Prediction, Diagnosis and Therapy for Gastric Cancer (JRF PDT GC), Tokyo, Japan.
                Author notes
                [† ]Correspondence should be addressed: K. Miki, Japan Research Foundation of Prediction, Diagnosis and Therapy for Gastric Cancer (JRF PDT GC), 1-17-2-604 Shirokane, Minato-ku, Tokyo 108-0072, Japan (e-mail: mikik@ 123456gastro-health-now.org ).

                (Communicated by Takashi SUGIMURA, M.J.A.)

                Article
                Publisher ID: pjab-87-405
                DOI: 10.2183/pjab.87.405
                PMC ID: 3171284
                PubMed ID: 21785258
                SO-VID: 622ef933-09aa-42e4-89ae-87095573c8b5
                Copyright © © 2011 The Japan Academy
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 13 December 2010
                Date accepted : 13 May 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Life sciences
                Keywords: gastric cancer,cancer screening,pepsinogen (pg) i, ii,anti-helicobacter pylori (hp) igg antibody,serum pepsinogen test method (pg method),screening for gastric cancer-risk (gastritis a, b, c, d) method (abc method)
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: gastric cancer, cancer screening, pepsinogen (pg) i, ii, anti-helicobacter pylori (hp) igg antibody, serum pepsinogen test method (pg method), screening for gastric cancer-risk (gastritis a, b, c, d) method (abc method)

                Comments

                Comment on this article

                scite_

                Similar content292

                See all similar

                Cited by100

                See all cited by

                Most referenced authors995

                See all reference authors