Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.
ADVANCED SEARCH
Log in
Top
Gastric Cancer
Published in: Gastric Cancer 1/2011

01-03-2011 | Review Article

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Authors: Hideyuki Ubukata, Hiroyuki Nagata, Takanobu Tabuchi, Satoru Konishi, Teruhiko Kasuga, Takafumi Tabuchi

Published in: Gastric Cancer | Issue 1/2011

Login to get access

Abstract

The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1–1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.
Literature
1.
Hussein NR. The association of dupA and Helicobacter pylori-related gastroduodenal diseases. Eur J Clin Microbiol Infect Dis. 2010;29:817–21.PubMedCrossRef
2.
Infection with Helicobacter pylori. IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 61. Schistosomes, liver flukes and Helicobacter pylori. Lyon: International Agency for Research on Cancer; 1994. p. 177–241.
3.
Labigne A, de Reuse H. Determinants of Helicobacter pylori pathogenicity. Infect Agents Dis. 1996;5:191–202.PubMed
4.
Graham DY. Helicobacter pylori infection in the pathogenesis of duodenal ulcer and gastric cancer: a model. Gastroenterology. 1997;113:1983–91.PubMedCrossRef
5.
Stemmermann GN, Fenoglio-Preiser C. Gastric carcinoma distal to the cardia: a review of the epidemiological pathology of the precursors to a preventable cancer. Pathology. 2002;34:494–503.PubMed
6.
Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S, Yamakido M, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med. 2001;345:784–9.PubMedCrossRef
7.
Fischer A, Clagett OT, McDonald JR. Coexistent duodenal ulcer and gastric malignancy. Surgery. 1947;21:168–74.PubMed
8.
Miwa M, Senoue I, Kikuchi K, Watanabe H, Nomiyama T, Suzuki S, et al. The coexistence of gastric cancer and duodenal ulcers. Tokai J Exp Clin Med. 1981;6:203–5.PubMed
9.
Take S, Mizuno M, Ishiki K, Nagahara Y, Yoshida T, Yokota K, et al. The effect of eradicating Helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease. Am J Gastroenterol. 2005;100:1037–42.PubMedCrossRef
10.
Kamada T, Hata J, Sugiu K, Kusunoki H, Ito M, Tanaka S, et al. Clinical features of gastric cancer discovered after successful eradication of Helicobacter pylori: results from a 9-year prospective follow-up study in Japan. Aliment Pharmacol Ther. 2005;21:1121–6.PubMedCrossRef
11.
Fuccio L, Zagari RM, Minardi ME, Bazzoli F. Systematic review: Helicobacter pylori for the prevention of gastric cancer. Aliment Pharmacol Ther. 2007;25:133–41.PubMedCrossRef
12.
Go MF, Graham DY. How does Helicobacter pylori cause duodenal ulcer disease: the bug, the host, or both? J Gastroenterol Hepatol. 1994;9(Suppl 1):S8–10.PubMedCrossRef
13.
14.
Atherton JC, Peek RM Jr, Tham KT, Cover TL, Blaser MJ. Clinical and pathological importance of heterogeneity in vacA, the vacuolating cytotoxin gene of Helicobacter pylori. Gastroenterology. 1997;112:92–9.PubMedCrossRef
15.
Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, Borodovsky M, et al. cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci USA. 1996;93:14648–53.PubMedCrossRef
16.
Prinz C, Schoniger M, Rad R, Becker I, Keiditsch E, Wagenpfeil S, et al. Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesion during chronic gastric inflammation. Cancer Res. 2001;61:1903–9.PubMed
17.
Li SD, Kersulyte D, Lindley IJ, Neelam B, Berg DE, Crabtree JE. Multiple genes in the left half of the cag pathogenicity island of Helicobacter pylori are required for tyrosine kinase-dependent transcription of interleukin-8 in gastric epithelial cells. Infect Immun. 1999;67:3893–9.PubMed
18.
Marrelli D, Pedrazzani C, Berardi A, Corso G, Neri A, Garosi L, et al. Negative Helicobacter pylori status is associated with poor prognosis in patients with gastric cancer. Cancer. 2009;115:2071–80.PubMedCrossRef
19.
Odenbreit S, Puls J, Sedlmaier B, Gerland E, Fischer W, Haas R. Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion. Science. 2000;287:1497–1500.PubMedCrossRef
20.
Huang JQ, Zheng GF, Sumanac K, Irvine EJ, Hunt RH. Meta-analysis of the relationship between cagA seropositivity and gastric cancer. Gastroenterology. 2003;125:1636–44.PubMedCrossRef
21.
Kuipers EJ, Perez-Perez GI, Meuwissen SG, Blaser MJ. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst. 1995;87:1777–80.PubMedCrossRef
22.
Hatakeyama M. Oncogenic mechanisms of the Helicobacter pylori CagA protein. Nat Rev Cancer. 2004;4:688–94.PubMedCrossRef
23.
Yamaoka Y, Kodama T, Kashima K, Graham DY, Sepulveda AR. Variants of the 3′ region of the cagA gene in Helicobacter pylori isolates from different H. pylori associated diseases. J Clin Microbiol. 1998;36:2258–63.PubMed
24.
Nomura AM, Perez-Perez GI, Lee J, Stemmermann G, Blaser MJ. Relation between Helicobacter pylori cagA status and risk of peptic ulcer disease. Am J Epidemiol. 2002;155:1054–9.PubMedCrossRef
25.
Lu H, Hsu PY, Graham DY, Yamaoka Y. Duodenal ulcer promoting gene of Helicobacter pylori. Gastroenterology. 2005;128:833–48.PubMedCrossRef
26.
Argent RH, Burette A, Miendje Deyi VY, Atherton JC. The presence of dupA in Helicobacter pylori is not significantly associated with duodenal ulceration in Belgium, South Africa, China, or North America. Clin Infect Dis. 2007;45:1204–6.PubMedCrossRef
27.
Nguyen LT, Uchida T, Tsukamoto Y, Kuroda A, Okimoto T, Kodama M, et al. Helicobacter pylori dupA gene is not associated with clinical outcomes in the Japanese population. Clin Microbiol Infect. 2010;16(8):1264–9.PubMedCrossRef
28.
Arachchi HS, Kalra V, Lal B, Bhatia V, Baba CS, Chakravarthy S, et al. Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population. Helicobacter. 2007;12:591–7.PubMedCrossRef
29.
Jung SW, Sugimoto M, Graham DY, Yamaoka Y. homB status of Helicobacter pylori as a novel marker to distinguish gastric cancer from duodenal ulcer. J Clin Microbiol. 2009;47:3241–5.PubMedCrossRef
30.
Camels S, Bereziat JC, Oshima H, Bartsch H. Bacterial formation of N-nitroso compounds in rats after omeprazole-induced achlorhydria. In: O’Neill IK, Chen J, Bartsch H, editors. Relevance to human cancer of N-nitroso compounds, tobacco smoke and mycotoxins (IARC scientific publication no. 105). Lyon: International Agency for Research on Cancer; 1991. p. 187–91.
31.
Sanduleanu S, Jonkers D, De Bruïne A, Hameeteman W, Stockbrügger RW. Double gastric infection with Helicobacter pylori and non-Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritis. Aliment Pharmacol Ther. 2001;15:1163–75.PubMedCrossRef
32.
Lamberts R, Creutzfeldt W, Strüber HG, Brunner G, Solcia E. Long-term omeprazole therapy in peptic ulcer disease: gastrin, endocrine cell growth, and gastritis. Gastroenterology. 1993;104:1356–70.PubMed
33.
Klinkenberg-Knol EC, Nelis F, Dent J, Snel P, Mitchell B, Prichard P, et al. Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safety, and influence on gastric mucosa. Gastroenterology. 2000;118:661–9.PubMedCrossRef
34.
Havu N. Enterochromaffin-like cell carcinoids of gastric mucosa in rats after life-long inhibition of gastric secretion. Digestion. 1986;35(Suppl 1):42–55.PubMedCrossRef
35.
Gillen D, McColl KE. Problem associated with the clinical use of proton pump inhibitors. Pharmacol Toxicol. 2001;89:281–6.PubMedCrossRef
36.
37.
Kuipers EJ, Sipponen P. Helicobacter pylori eradication for the prevention of gastric cancer. Helicobacter. 2006;11(Suppl 1):52–7.PubMedCrossRef
38.
Lundegårdh G, Ekbom A, McLaughlin JK, Nyrén O. Gastric cancer risk after vagotomy. Gut. 1994;35:946–9.PubMedCrossRef
39.
Møller H, Nissen A, Mosbech J. Use of cimetidine and other peptic ulcer drugs in Denmark 1977–1990 with analysis of the risk of gastric cancer among cimetidine users. Gut. 1992;33:1166–9.PubMedCrossRef
40.
41.
Muscroft TJ, Youngs DJ, Burdon DW, Keighley. Cimetidine is unlikely to increase formation of intragastric N-nitroso-compounds in patients taking a normal diet. Lancet. 1981;I:408–10.CrossRef
42.
Lin CY, Bai DJ, Yuan HY, Wang K, Yang GL, Hu MB, et al. Perioperative cimetidine administration promotes peripheral blood lymphocytes and tumor infiltrating lymphocytes in patients with gastrointestinal cancer: results of a randomized controlled clinical trial. World J Gastroenterol. 2004;10:136–42.PubMed
43.
Milito AD, Fais S. Proton pump inhibitor may reduce tumour resistance. Scand J Gastroenterol. 2005;6:1049–54.
44.
Dillman RO, Soori G, DePriest C, Nayak SK, Beutel LD, de Leon C, et al. Treatment of human solid malignancies with autologous activated lymphocytes and cimetidine: a phase II trial of the Cancer Biotherapy Research Group. Cancer Biother Radiopharm. 2003;18:727–33.PubMedCrossRef
45.
Jiang CG, Liu FR, Li JB, Xu HM. Cimetidine induces apoptosis in gastric cancer cells in vitro and inhibits tumor growth in vivo. Oncol Rep. 2010;23:693–700.PubMedCrossRef
46.
Langman MJS, Dunn JA, Whiting JL, Burton A, Hallissey MT, Fielding JWL, et al. Prospective, double-blind, placebo-controlled randomized trial of cimetidine in gastric cancer. Br J Cancer. 1999;81:1356–62.PubMedCrossRef
47.
Gridley G, McLaughlin JK, Ekbom A, Klareskog L, Adami HO, Hacker DG, et al. Incidence of cancer among patients with rheumatoid arthritis. J Natl Cancer Inst. 1993;85:307–11.PubMedCrossRef
48.
Thun MJ, Namboodiri MM, Calle EE, Flanders WD, Health CW Jr. Aspirin use and risk of fatal cancer. Cancer Res. 1993;53:1322–7.PubMed
49.
Wang WH, Huang JQ, Zheng GF, Lam SK, Karlberg J, Wong BC. Non-steroidal anti-inflammatory drug use and the risk of gastric cancer: a systematic review and meta-analysis. J Natl Cancer Inst. 2003;95:1784–91.PubMed
50.
Shirin H, Moss SF, Stark B, Weinstein IB, Holt PR, Sordillo EM. Inhibition of Helicobacter pylori growth by sulindac. Gastroenterology. 2000;119:A4931 (abstract).
51.
Takahashi M, Katayama Y, Takada H, Kuwayama H, Terano A. The effect of NSAIDs and a COX-2 specific inhibitor on Helicobacter pylori-induced PGE2 and HGF in human gastric fibroblasts. Aliment Pharmacol Ther. 2000;14(Suppl 1):44–9.PubMedCrossRef
52.
Hudson N, Balsitis M, Filipowicz F, Hawkey CJ. Effect of Helicobacter pylori colonization on gastric mucosal eicosanoid synthesis in patients taking non-steroidal anti-inflammatory drugs. Gut. 1993;34:748–51.PubMedCrossRef
53.
Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. N Engl J Med. 1999;340:1888–99.PubMedCrossRef
54.
Garcia Rodriguez LA, Lagergren J, Lindblad M. Gastric acid suppression and risk of oesophageal and gastric adenocarcinoma: a nested case control study in the UK. Gut. 2006;55:1538–44.PubMedCrossRef
55.
McColl KE. Acid inhibitory medication and risk of gastric and oesophageal cancer. Gut. 2006;55:1532–3.PubMedCrossRef
56.
Correa P, Cuello C, Fajardo LF, Haenszel W, Bolaños O, de Ramirez B. Diet and gastric cancer: nutrition survey in a high-risk area. Natl Cancer Inst. 1983;70:673–8.
57.
Parsonnet J, Friedman GD, Vandersteen DP, Chang Y, Vogelman JH, Orentreich N, et al. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991;325:1127–31.PubMedCrossRef
58.
Correa P, Piazuelo MB, Camargo MC. The future of gastric cancer prevention. Gastric Cancer. 2004;7:9–16.PubMedCrossRef
59.
Kobayashi M, Tsubono Y, Sasazuki S, Sasaki S, Tsugane S. Vegetables, fruit and risk of gastric cancer in Japan: a 10-year follow-up of the JPHC Study Cohort I. Int J Cancer. 2002;102:39–44.PubMedCrossRef
60.
Chen TS, Lee YC, Li FY, Chang FY. Smoking and hyperpepsinogenemia are associated with increased risk for duodenal ulcer in Helicobacter pylori-infected patients. J Clin Gastroenterol. 2005;39:699–703.PubMedCrossRef
61.
Sierra R, Une C, Ramirez V, Gonzalez MI, Ramirez JA, de Mascarel A, et al. Association of serum pepsinogen with atrophic body gastritis in Costa Rica. Clin Exp Med. 2006;6:72–9.PubMedCrossRef
62.
Faber K. Gastritis and its consequences. London: Oxford University Press; 1935.
63.
Nyfeldt A, Vimtrup B. Gastritis acuta bei diphtheria faucium. Acta Med Scand. 1932;78:447–83.CrossRef
64.
Schoen AM. Acute gastritis. In: Bockus HL, editor. Gastroenterology. 2nd ed. Philadelphia: Saunders; 1963. p. 351–67.
65.
Suzuki M, Miura S, Suematsu M, Fukumura D, Kurose I, Suzuki H, et al. Helicobacter pylori-associated ammonia production enhances neutrophil-dependent gastric mucosal cell injury. Am J Physiol. 1992;263:G719–25.PubMed
66.
Murakami M, Asagoe K, Dekigai H, Kusaka S, Saita H, Kita T. Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage. Dig Dis Sci. 1995;40:268–73.PubMedCrossRef
67.
Takashima M, Furuta T, Hanai H, Sugimura H, Kaneko E. Effects of Helicobacter pylori infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils. Gut. 2001;48:765–73.PubMedCrossRef
68.
Esplugues JV, Martinez-Cuesta MA, Barrachina MD, Calatayud S, Whittle BJ. Involvement of endogenous nitric oxide in the inhibition by endotoxin and interleukin-1 beta of gastric acid secretion. J Gastroenterol Hepatol. 1994;9(Suppl 1):S45–9.PubMedCrossRef
69.
Kondo S, Shinomura Y, Kanayama S, Kawabata S, Miyazaki Y, Imamura I, et al. Interleukin-1 beta of pentagastrin-stimulated rat gastric acid secretion. Br J Pharmacol. 1993;108:9–10.
70.
El-Omar EM, Rabkin CS, Gammon MD, Vaughan TL, Risch HA, Schoenberg JB, et al. Increased risk of noncardia gastric cancer associated with proinflammatory cytokine gene polymorphisms. Gastroenterology. 2003;124:1193–201.PubMedCrossRef
71.
Furuta T, El-Omar EM, Xiao F, Shirai N, Takashima M, Sugimura H. Interleukin 1 beta polymorphisms increase risk of hypochlorhydria and atrophic gastritis and reduce risk of duodenal ulcer recurrence in Japan. Gastroenterology. 2002;123:92–105.PubMedCrossRef
72.
Figueiredo C, Machado JC, Pharoah P, Seruca R, Sousa S, Carvalho R, et al. Helicobacter pylori and interleukin 1 genotyping: an opportunity to identify high risk individuals for gastric carcinoma. J Natl Cancer Inst. 2002;94:1680–7.PubMed
73.
Camargo MC, Mera R, Correa P, Peek RM Jr, Fontham ET, Goodman KJ, et al. Interleukin-1 beta and interleukin-1 receptor antagonist gene polymorphisms and gastric cancer: a meta-analysis. Cancer Epidemiol Biomarkers Prev. 2006;15:1674–87.PubMedCrossRef
74.
Zambon CF, Basso D, Navaglia F, Belluco C, Falda A, Fogar P, et al. Pro- and anti-inflammatory cytokines gene polymorphisms and Helicobacter pylori infection: interactions influence outcome. Cytokine. 2005;29:141–52.PubMedCrossRef
75.
El-Omar EM, Carrington M, Chow WH, McColl KE, Bream JH, Young HA, et al. Interleukin-1 polymorphisms associated with increased risk of gastric cancer. Nature. 2000;404:398–402.PubMedCrossRef
76.
Kato S, Onda M, Yamada S, Matsuda N, Tokunaga A, Matsukura N. Association of the interleukin-1 beta genetic polymorphism and gastric cancer risk in Japanese. J Gastroenterol. 2001;36:696–9.PubMedCrossRef
77.
Lee SG, Kim B, Choi W, Lee I, Choi J, Song K, et al. Lack of association between pro-inflammatory genotypes of the interleukin-1 (IL-1B-31 C/+ and IL-1RN*2/*2) and gastric cancer/duodenal ulcer in Korean population. Cytokine. 2003;21:167–71.PubMedCrossRef
78.
Gatti LI, Burbano RR, de Assumpção PP, Smith M de A, Payão SL. Interleukin-1 beta polymorphisms, Helicobacter pylori infection in individuals from Northern Brazil with gastric adenocarcinoma. Clin Exp Med. 2004;4:93–8.PubMedCrossRef
79.
Kamangar F, Abnet CC, Hutchinson AA, Newschaffer CJ, Helzlsouer K, Shugart YY, et al. Polymorphisms in inflammation-related genes and risk of gastric cancer (Finland). Cancer Causes Control. 2006;17:117–25.PubMedCrossRef
80.
Chang YW, Oh HC, Jang JY, Hwangbo Y, Lee JW, Lee J, et al. IL-1B and IL-8, matrix metalloproteinases 3, and pepsinogen secretion before and after H. pylori eradication in gastroduodenal phenotypes. Scand J Gastroenterol. 2008;43:1184–93.PubMedCrossRef
81.
Partida-Rodríguez O, Torres J, Flores-Luna L, Camorlonga M, Nieves-Ramírez M, Lazcano E, et al. Polymorphisms in TNF and HSP-70 show a significant association with gastric cancer and duodenal ulcer. Int J Cancer. 2010;126:1861–8.PubMed
82.
Jones MK, Kawanaka H, Baatar D, Szabó IL, Tsugawa K, Pai R, et al. Gene therapy for gastric ulcers with single local injection of naked DNA encoding VEGF and angioprotein-1. Gastroenterology. 2001;121:1040–7.PubMedCrossRef
83.
Suzuki N, Takahashi S, Okabe S. Relationship between vascular endothelial growth factor and angiogenesis in spontaneous and indomethacin-delayed healing of acetic acid-induced gastric ulcer in rats. J Physiol Pharmacol. 1998;49:515–27.PubMed
84.
Takahashi Y, Clearly KR, Mai M, Kitadai Y, Bucana CD, Ellis LM. Significance of vessel count and vascular endothelial growth factor and its receptor (KDR) in intestinal-type gastric cancer. Clin Cancer Res. 1996;2:1679–84.PubMed
85.
Maeda K, Kang SM, Onoda N, Ogawa M, Kato Y, Sawada T, et al. Vascular endothelial growth factor expression in preoperative biopsy specimens correlates with disease recurrence in patients with early gastric carcinoma. Cancer. 1999;86:566–71.PubMedCrossRef
86.
Feng CW, Wang LD, Jiao LH, Liu B, Zheng S, Xie XJ. Expression of p53, inducible nitric oxide synthase and vascular endothelial growth factor in gastric precancerous and cancerous lesions: correlation with clinical features. BMC Cancer. 2000;29:2–8.
87.
Tahara T, Shibata T, Nakamura M, Yamashita H, Yoshioka D, Hirata I, et al. Effect of polymorphisms in the 3′ untranslated region (3′-UTR) of vascular endothelial growth factor gene on gastric cancer and peptic ulcer diseases in Japan. Mol Carcinog. 2009;48:1030–7.PubMedCrossRef
88.
Takatsu S, Tsuchiya H, Kitamura A, Yoshida S, Ito M, Sakurai Y, et al. Detection of early gastric cancer by panendoscopy. Jpn J Clin Oncol. 1984;14:243–52.
89.
Hosokawa O, Kaizaki Y, Nakaya T, Hinoshita T, Watanabe K, Douden K, et al. Retrospective study of endoscopic findings: 250 cases of gastric cancer. Dig Endosc. 2000;12:136–40.CrossRef
90.
Mabe K, Takahashi M, Oizumi H, Tsukuma H, Shibata A, Fukase K, et al. Does Helicobacter pylori eradication therapy for peptic ulcer prevent gastric cancer? World J Gastroenterol. 2009;14:4290–7.CrossRef
91.
Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. 1992;52:6735–40.PubMed
92.
Khulusi S, Badve S, Patel P, Lloyd R, Marrero JM, Finlayson C, et al. Pathogenesis of gastric metaplasia of the human duodenum: role of Helicobacter pylori, gastric acid, and ulceration. Gastroenterology. 1996;110:452–8.PubMedCrossRef
93.
Sipponen P, Ranta P, Helske T, Kaariainen I, Maki T, Linnala A, et al. Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case–control study. Scand J Gastroenterol. 2002;37:785–91.PubMed
94.
Wu MS, Chen CJ, Lin JT. Host-environmental interactions: their impact on progression from gastric inflammation to carcinogenesis and on development of new approaches to prevent and treat gastric cancer. Cancer Epidemiol Biomarkers Prev. 2005;14:1878–82.PubMedCrossRef
95.
Hwang IR, Kodama T, Kikuchi S, Sakai K, Peterson LE, Graham DY, et al. Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1β production in Helicobacter pylori infection. Gastroenterology. 2002;123:1793–803.PubMedCrossRef
96.
97.
Ames BN, Gold LS. Too many rodent carcinogens: mitogenesis increases mutagenesis. Science. 1990;249:970–1.PubMedCrossRef
98.
Kubo T, Imai T. Intestinal metaplasia of gastric mucosa in autopsy materials in Hiroshima and Yamaguchi districts. Gann. 1971;62:49–53.PubMed
99.
Solcia E, Fiocca R, Luinetti O, Villani L, Padovan L, Calistri D, et al. Intestinal and diffuse gastric cancers arise in a different background of Helicobacter pylori gastritis through different gene involvement. Am J Surg Pathol. 1996;20(Suppl 1):S8–22.PubMed
Metadata
Title
Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer
Authors
Hideyuki Ubukata
Hiroyuki Nagata
Takanobu Tabuchi
Satoru Konishi
Teruhiko Kasuga
Takafumi Tabuchi
Publication date
01-03-2011
Publisher
Springer Japan
Published in
Gastric Cancer / Issue 1/2011
Print ISSN: 1436-3291
Electronic ISSN: 1436-3305
DOI
https://doi.org/10.1007/s10120-011-0005-9

Other articles of this Issue 1/2011

Gastric Cancer 1/2011 Go to the issue

Original Article

Management of adjuvant S-1 therapy after curative resection of gastric cancer: dose reduction and treatment schedule modification

Original Article

Randomized phase III study comparing the efficacy and safety of irinotecan plus S-1 with S-1 alone as first-line treatment for advanced gastric cancer (study GC0301/TOP-002)

Original Article

Clinical impact of a strategy involving endoscopic submucosal dissection for early gastric cancer: determining the optimal pathway

Editorial

Irinotecan is inactive as a first-line treatment, but plays an important part in gastric cancer treatment

Original Article

Increased Slug and decreased E-cadherin expression is related to poor prognosis in patients with gastric cancer

Original Article

Depth-predicting score for differentiated early gastric cancer
Live Webinar | 27-06-2024 | 18:00 (CEST)

Keynote webinar | Spotlight on medication adherence

Reserve your place

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

WHO estimates that half of all patients worldwide are non-adherent to their prescribed medication. The consequences of poor adherence can be catastrophic, on both the individual and population level.

Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.

Prof. Kevin Dolgin
Prof. Florian Limbourg
Prof. Anoop Chauhan
Developed by: Springer Medicine
Obesity Clinical Trial Summary

At a glance: The STEP trials

Read more

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Highlights from the ACC 2024 Congress

Year in Review: Pediatric cardiology

Pediatric Cardiology Video

Watch Dr. Anne Marie Valente present the last year's highlights in pediatric and congenital heart disease in the official ACC.24 Year in Review session.

Year in Review: Pulmonary vascular disease

Cardiopulmonary Comorbidity Video

The last year's highlights in pulmonary vascular disease are presented by Dr. Jane Leopold in this official video from ACC.24.

Year in Review: Valvular heart disease

Valvular Heart Disease Video

Watch Prof. William Zoghbi present the last year's highlights in valvular heart disease from the official ACC.24 Year in Review session.

Year in Review: Heart failure and cardiomyopathies

Heart Failure Video

Watch this official video from ACC.24. Dr. Biykem Bozkurt discusses last year's major advances in heart failure and cardiomyopathies.

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Heart Failure Video

Watch this official video from ACC.24. Dr. Biykem Bozkurt discusses last year's major advances in heart failure and cardiomyopathies.

Watch now

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

16-04-2024 Type 2 Diabetes News

Incentivised to exercise

11-04-2024 Lifestyle Modifications News

New intervention for STEMI-related cardiogenic shock

10-04-2024 Myocardial Infarction News

» View more highlights on the ACC 2024 congress hub page

Image Credits