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Pu K, Feng Y, Tang Q, Yang G, Xu C. Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence. Front Oncol 2024; 14:1333623. [PMID: 38444674 PMCID: PMC10912593 DOI: 10.3389/fonc.2024.1333623] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/05/2023] [Accepted: 02/02/2024] [Indexed: 03/07/2024] Open
Abstract
Due to rapid research expansion on dietary factors and development of cancer prevention guidelines, the field of dietary pattern and its relationship to cancer risk has gained more focus. Numerous epidemiology studies have reported associations between Gastric Cancer (GC) and both data-driven posteriori dietary pattern and priori dietary pattern defined by predetermined dietary indexes. As dietary patterns have evolved, a series of patterns based on biological markers has advanced, offering deeper insights into the relationship between diet and the risk of cancer. Although researches on dietary patterns and cancer risk are booming, there is limited body of literature focusing specifically on GC. In this study, we compare the similarities and differences among the specific components of dietary patterns and indices, summarize current state of knowledge regarding dietary patterns related to GC and illustrate their potential mechanisms for GC prevention. In conclusion, we offer suggestions for future research based on the emerging themes within this rapidly evolving field.
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Affiliation(s)
- Ke Pu
- Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, Sichuan, China
- Department of Gastroenterology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China
| | - Yang Feng
- Department of Neurosurgery, Xi’an No.3 Hospital, The Affiliated Hospital of Northwest University, Xi’an, Shaanxi, China
| | - Qian Tang
- Statesboro Office, Southeast Medical Group, Atlanta, GA, United States
| | - Guodong Yang
- Department of Gastroenterology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China
| | - Chuan Xu
- Department of Oncology & Cancer Institute, Sichuan Academy of Medical Sciences, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China
- Department of Laboratory Medicine and Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China
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Mizukami A, Kawaguchi Y, Shoda K, Akaike H, Saito R, Maruyama S, Shiraishi K, Furuya S, Amemiya H, Kawaida H, Sudo M, Kono H, Ichikawa D. Postoperative Remission of Diabetes Mellitus After Gastrectomy in Patients With Diabetes Mellitus and Gastric Cancer. In Vivo 2023; 37:2808-2814. [PMID: 37905629 PMCID: PMC10621454 DOI: 10.21873/invivo.13394] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/16/2023] [Revised: 07/21/2023] [Accepted: 07/25/2023] [Indexed: 11/02/2023]
Abstract
BACKGROUND/AIM We investigated the postoperative treatment status for diabetes mellitus and perioperative HbA1c levels in patients with diabetes mellitus and examined the effects of clinical factors on the remission of diabetes mellitus. PATIENTS AND METHODS In this study, 126 patients with gastric cancer were considered to have diabetes mellitus preoperatively, of whom 79 were treated with oral antidiabetic drugs and/or insulin treatment. We compared diabetic treatment status and HbA1c values between the preoperative and postoperative periods in patients who underwent gastrectomy and examined the effects of clinical factors on improving diabetes mellitus. RESULTS Of the 79 patients treated preoperatively for diabetes mellitus, 34 (43%) discontinued all medications for diabetes mellitus and for 37 (47%) the therapeutic dose was reduced or switched from insulin to oral antidiabetic drugs. Total gastrectomy was an independent factor for remission of antidiabetic treatments after gastrectomy. Concerning HbA1c levels, only the absence of preoperative insulin use was an independent factor for improvement. However, reconstruction was not a significantly correlated factor for the improvement of postoperative HbA1c levels and reduction of antidiabetic medications after distal gastrectomy. CONCLUSION Almost all patients discontinued or had their dose of antidiabetic medications reduced after gastrectomy in clinical practice, and special attention should be paid in the management methods for diabetes mellitus in patients who underwent total gastrectomy for gastric cancer.
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Affiliation(s)
- Akihito Mizukami
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Yoshihiko Kawaguchi
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Kastutoshi Shoda
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Hidenori Akaike
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Ryo Saito
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Suguru Maruyama
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Kensuke Shiraishi
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Shinji Furuya
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Hidetake Amemiya
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Hiromichi Kawaida
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Makoto Sudo
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Hiroshi Kono
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
| | - Daisuke Ichikawa
- First Department of Surgery, Faculty of Medicine University of Yamanashi, Yamanashi, Japan
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Mahmood R, Voisin A, Olof H, Khorasaniha R, Lawal SA, Armstrong HK. Host Microbiomes Influence the Effects of Diet on Inflammation and Cancer. Cancers (Basel) 2023; 15:521. [PMID: 36672469 PMCID: PMC9857231 DOI: 10.3390/cancers15020521] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/23/2022] [Revised: 01/12/2023] [Accepted: 01/13/2023] [Indexed: 01/19/2023] Open
Abstract
Cancer is the second leading cause of death globally, and there is a growing appreciation for the complex involvement of diet, microbiomes, and inflammatory processes culminating in tumorigenesis. Although research has significantly improved our understanding of the various factors involved in different cancers, the underlying mechanisms through which these factors influence tumor cells and their microenvironment remain to be completely understood. In particular, interactions between the different microbiomes, specific dietary factors, and host cells mediate both local and systemic immune responses, thereby influencing inflammation and tumorigenesis. Developing an improved understanding of how different microbiomes, beyond just the colonic microbiome, can interact with dietary factors to influence inflammatory processes and tumorigenesis will support our ability to better understand the potential for microbe-altering and dietary interventions for these patients in future.
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Affiliation(s)
- Ramsha Mahmood
- Department of Internal Medicine, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
| | - Athalia Voisin
- Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
| | - Hana Olof
- Department of Immunology, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
| | - Reihane Khorasaniha
- Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
| | - Samuel A. Lawal
- Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
| | - Heather K. Armstrong
- Department of Internal Medicine, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
- Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
- Department of Immunology, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
- Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
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Wroblewski LE, Peek RM. Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development. Curr Top Microbiol Immunol 2023; 444:25-52. [PMID: 38231214 PMCID: PMC10924282 DOI: 10.1007/978-3-031-47331-9_2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2024]
Abstract
The human pathogen Helicobacter pylori is the strongest known risk factor for gastric disease and cancer, and gastric cancer remains a leading cause of cancer-related death across the globe. Carcinogenic mechanisms associated with H. pylori are multifactorial and are driven by bacterial virulence constituents, host immune responses, environmental factors such as iron and salt, and the microbiota. Infection with strains that harbor the cytotoxin-associated genes (cag) pathogenicity island, which encodes a type IV secretion system (T4SS) confer increased risk for developing more severe gastric diseases. Other important H. pylori virulence factors that augment disease progression include vacuolating cytotoxin A (VacA), specifically type s1m1 vacA alleles, serine protease HtrA, and the outer-membrane adhesins HopQ, BabA, SabA and OipA. Additional risk factors for gastric cancer include dietary factors such as diets that are high in salt or low in iron, H. pylori-induced perturbations of the gastric microbiome, host genetic polymorphisms, and infection with Epstein-Barr virus. This chapter discusses in detail host factors and how H. pylori virulence factors augment the risk of developing gastric cancer in human patients as well as how the Mongolian gerbil model has been used to define mechanisms of H. pylori-induced inflammation and cancer.
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Affiliation(s)
- Lydia E Wroblewski
- Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA
| | - Richard M Peek
- Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
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Khairan P, Sobue T, Eshak ES, Zha L, Kitamura T, Sawada N, Iwasaki M, Inoue M, Yamaji T, Iso H, Tsugane S. Association of B Vitamins and Methionine Intake with the Risk of Gastric Cancer: The Japan Public Health Center-based Prospective Study. Cancer Prev Res (Phila) 2021; 15:101-110. [PMID: 34815313 DOI: 10.1158/1940-6207.capr-21-0224] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/25/2021] [Revised: 10/14/2021] [Accepted: 11/16/2021] [Indexed: 12/24/2022]
Abstract
Dietary intake of B vitamins and methionine might associate with carcinogenesis due to their role in DNA synthesis and methylation. Owing to the previous inconsistent findings on gastric cancer risk, we aimed to examine the associations between dietary intakes of B vitamins and methionine and the risk of gastric cancer, according to sodium intake.We included 86,820 Japanese individuals who completed a validated food frequency questionnaire with 138 food items in the Japan Public Health Center-based Prospective Study. Cox proportional hazards regression was used to obtain HRs and 95% confidence intervals (CI) of gastric cancer according to separate intakes of folate, vitamin B6, vitamin B12, and methionine after adjusting for confounding factors, including Helicobacter pylori and atrophic gastritis in the subgroup analysis.We identified 2,269 gastric cancer cases within a median of 15.4 years of follow-up. We found no association between any of the dietary intakes of folate, vitamin B6, vitamin B12, or methionine with the risk of gastric cancer. In the stratified analysis by sodium intake, we observed a positive association between folate intake and risk of gastric cancer among participants with a high sodium intake (≥4.5 g/day) [HR = 1.28 (95% CI, 1.06-1.56), P trend = 0.001; P interaction = 0.02]. Meanwhile, there was no association between folate intake and risk of gastric cancer among participants with low sodium intake (<4.5 g/day) [HR = 0.94 (95% CI, 0.73-1.21), P trend = 0.49].In conclusion, we found no association between any dietary intakes of folate, vitamin B6, vitamin B12, and methionine with the risk of gastric cancer. PREVENTION RELEVANCE: The increased intake of B vitamins and methionine in populations with adequate dietary intake of these nutrients showed no association with the risk of gastric cancer.
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Affiliation(s)
- Paramita Khairan
- Division of Environmental Medicine and Population Sciences, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.,Department of Internal Medicine, Faculty of Medicine, Universitas Muhammadiyah Jakarta, Jakarta, Indonesia
| | - Tomotaka Sobue
- Division of Environmental Medicine and Population Sciences, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
| | - Ehab Salah Eshak
- Department of Public Health and Preventive Medicine, Faculty of Medicine, Minia University, Minya, Egypt.,Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
| | - Ling Zha
- Division of Environmental Medicine and Population Sciences, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
| | - Tetsuhisa Kitamura
- Division of Environmental Medicine and Population Sciences, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
| | - Norie Sawada
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Chuo-ku, Tokyo, Japan
| | - Motoki Iwasaki
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Chuo-ku, Tokyo, Japan
| | - Manami Inoue
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Chuo-ku, Tokyo, Japan
| | - Taiki Yamaji
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Chuo-ku, Tokyo, Japan
| | - Hiroyasu Iso
- Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
| | - Shoichiro Tsugane
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Chuo-ku, Tokyo, Japan
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Abstract
Gastric cancer is the fifth most common cause of cancer and the third leading cause of cancer-related deaths globally. The number of gastric cancer-related deaths is only projected to increase, attributable primarily to the expanding aging population. Prevention is a mainstay of gastric cancer control programs, particularly in the absence of accurate, noninvasive modalities for screening and early detection, and the absence of an infrastructure for this purpose in the majority of countries worldwide. Herein, we discuss the evidence for several chemopreventive agents, along with putative mechanisms. There remains a clear, unmet need for primary chemoprevention trials for gastric cancer.
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Affiliation(s)
- Shailja C. Shah
- Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, Vanderbilt University Medical Center, 1030C MRB IV, 2215 Garland Avenue, Nashville, TN 37232-0252, USA;,Veterans Affairs Tennessee Valley Health System, Nashville Campus, Nashville, TN, USA,Corresponding author:
| | - Richard M. Peek
- Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, Vanderbilt University Medical Center, 1030C MRB IV, 2215 Garland Avenue, Nashville, TN 37232-0252, USA
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Vahid F, Davoodi SH. Nutritional Factors Involved in the Etiology of Gastric Cancer: A Systematic Review. Nutr Cancer 2020; 73:376-390. [PMID: 32336147 DOI: 10.1080/01635581.2020.1756353] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
CONTEXT Since treatment options for GC are limited, the best and most effective way is to try to reduce the incidences and understanding prevention strategies. OBJECTIVE The success in prevention strategies depends on understanding etiologic mechanisms. Our goal is to identify the major nutritional risk factors for GC, and we will examine the controversial evidence. DATA SOURCES We used Pub Med, Google Scholar, Scopus, Science Direct, Elsevier, Springer, and MEDLINE databases for extracting articles. DATA EXTRACTION Human studies published in English from 1997to2018 were included. Two reviewers other than authors initially assessed abstract of 742 papers and 248papers were selected for future assessments. After full review and consideration of the inclusion and exclusion criteria, we used 85 articles. RESULTS Dietary salt is a strong independent risk for GC whereas alcohol is most likely a risk only in the presence of heavy alcohol consumption. Red meat and high-fat diet increase the risk of developing GC but fresh fruits, vegetables and certain micronutrients like selenium and vitamin C are protective. CONCLUSION Some nutrients such as selenium, vitamin C, folate, iron, and zinc are involved in the etiology of GC. On the other hand; salt, fats, alcohol, red meat, and pepper were reported to be risk factors for GC. Since the GC is a heterogeneous malignancy and multiple factors are involved in its genesis.
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Affiliation(s)
- Farhad Vahid
- Department of Nutritional Sciences, School of Health, Arak University of Medical Sciences, Arak, Iran
| | - Sayed Hossein Davoodi
- Faculty of Nutrition Sciences and Food Technology, Department of Nutritional Sciences, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran.,Cancer Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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8
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Key TJ, Bradbury KE, Perez-Cornago A, Sinha R, Tsilidis KK, Tsugane S. Diet, nutrition, and cancer risk: what do we know and what is the way forward? BMJ 2020; 368:m511. [PMID: 32139373 PMCID: PMC7190379 DOI: 10.1136/bmj.m511] [Citation(s) in RCA: 123] [Impact Index Per Article: 24.6] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Affiliation(s)
- Timothy J Key
- Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK
| | - Kathryn E Bradbury
- National Institute for Health Innovation, School of Population Health, University of Auckland, Auckland, New Zealand
| | - Aurora Perez-Cornago
- Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK
| | - Rashmi Sinha
- Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
| | - Konstantinos K Tsilidis
- Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
| | - Shoichiro Tsugane
- Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
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Wu D, Cao M, Li N, Zhang A, Yu Z, Cheng J, Xie X, Wang Z, Lu S, Yan S, Zhou J, Peng J, Zhao J. Effect of trimethylamine N-oxide on inflammation and the gut microbiota in Helicobacter pylori-infected mice. Int Immunopharmacol 2019; 81:106026. [PMID: 31759863 DOI: 10.1016/j.intimp.2019.106026] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/14/2019] [Revised: 10/14/2019] [Accepted: 11/04/2019] [Indexed: 02/07/2023]
Abstract
Diet is one of the factors contributing to symptom of Helicobacter pylori (H. pylori) infection. Trimethylamine N-oxide (TMAO), a diet-related microbial metabolite, is associated with inflammatory and metabolic diseases. The aim of this study is to investigate the effects of TMAO intake on inflammation and gut microbiota composition in H. pylori-infected mice via 16S rRNA sequencing and biochemical analyses. The in vitro experiments showed that TMAO not only increased the expression of growth- and metabolism-associated genes and the urease activity of H. pylori, but increased the production of virulence factors. Moreover, TMAO intake increased the production of inflammatory markers and reduced the richness and diversity of the gut microbiota in H. pylori-infected mice. Further analysis showed that TMAO increased the relative abundance of Escherichia_Shigella in H. pylori-infected mice, which had positive correlation with the levels of LPS, CRP, and CXCL1. Collectively, our results suggest that TMAO may aggravate H. pylori-induced inflammation by increasing the viability and virulence of H. pylori and may aggravate inflammation in association with the gut microbiota in H. pylori-infected mice. This study may provide a novel insight into the mechanism for the effect of diet-derived metabolites such as TMAO on H. pylori-induced disease development.
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Affiliation(s)
- Daoyan Wu
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China; Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, PR China
| | - Mei Cao
- Core Laboratory, School of Medicine, Sichuan Provincial People's Hospital Affiliated to University of Electronic Science and Technology of China, Chengdu 610072, PR China
| | - Ningzhe Li
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Andong Zhang
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Zhihao Yu
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Juan Cheng
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Xiulan Xie
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Zeyu Wang
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Shaofei Lu
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Shiying Yan
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Jie Zhou
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Jingshan Peng
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China
| | - Jian Zhao
- Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Sciences, Sichuan University, Chengdu 610064, PR China.
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Peng C, Li NS, Hu Y, Lu NH. Impact factors that modulate gastric cancer risk in Helicobacter pylori-infected rodent models. Helicobacter 2019; 24:e12580. [PMID: 30950162 DOI: 10.1111/hel.12580] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/15/2018] [Revised: 02/08/2019] [Accepted: 02/26/2019] [Indexed: 12/24/2022]
Abstract
Gastric cancer causes a large social and economic burden to humans. Helicobacter pylori (H pylori) infection is a major risk factor for distal gastric cancer. Detailed elucidation of H pylori pathogenesis is significant for the prevention and treatment of gastric cancer. Animal models of H pylori-induced gastric cancer have provided an invaluable resource to help elucidate the mechanisms of H pylori-induced carcinogenesis as well as the interaction between host and the bacterium. Rodent models are commonly used to study H pylori infection because H pylori-induced pathological processes in the stomachs of rodents are similar to those in the stomachs of humans. The risk of gastric cancer in H pylori-infected animal models is greatly dependent on host factors, bacterial determinants, environmental factors, and microbiota. However, the related mechanisms and the effects of the interactions among these impact factors on gastric carcinogenesis remain unclear. In this review, we summarize the impact factors mediating gastric cancer risk when establishing H pylori-infected animal models. Clarifying these factors and their potential interactions will provide insights to construct animal models of gastric cancer and investigate the in-depth mechanisms of H pylori pathogenesis, which might contribute to the management of H pylori-associated gastric diseases.
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Affiliation(s)
- Chao Peng
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China
| | - Nian-Shuang Li
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China
| | - Yi Hu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China
| | - Nong-Hua Lu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China
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Saberi S, Piryaei A, Mirabzadeh E, Esmaeili M, Karimi T, Momtaz S, Abdirad A, Sodeifi N, Mohagheghi MA, Baharvand H, Mohammadi M. Immunohistochemical Analysis of LGR5 and TROY Expression in Gastric Carcinogenesis Demonstrates an Inverse Trend. IRANIAN BIOMEDICAL JOURNAL 2019; 23:107-120. [PMID: 30501144 PMCID: PMC6707110 DOI: 10.29252/.23.2.107] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 09/15/2018] [Revised: 10/07/2018] [Accepted: 09/08/2018] [Indexed: 11/05/2022]
Abstract
BACKGROUND Two of the Wnt signaling pathway target genes, tumor necrosis factor receptor family member (TROY) and leucine-rich G-protein coupled receptor (LGR5), are involved in the generation and maintenance of gastrointestinal epithelium. A negative modulatory role has recently been assigned to TROY, in this pathway. Here, we have examined their simultaneous expression in gastric carcinogenesis. METHODS Tumor and paired adjacent tissues of intestinal-type gastric cancer (GC) patients (n = 30) were evaluated for LGR5 and TROY expression by immunohistochemistry. The combination of the percentage of positively¬ stained cells and the intensity of staining was defined as the composite score and compared between groups. The obtained findings were re-evaluated in a mouse model. RESULTS TROY expression in the tumor tissue was significantly lower than that of the adjacent tissue (2.5 ± 0.9 vs. 3.3 ± 0.9, p = 0.004), which was coincident with higher LGR5 expression (3.6 ± 1.1 vs. 2.7 ± 0.9, p = 0.001). This observation was prominent at stages II/III of GC, leading to a statistically significant mean difference of expression between these two molecules (p = 0.005). In the H. pylori infected-mouse model, this inverse expression was observed in transition from early (8-16 w) to late (26-50 w) time points, post treatment (p = 0.002). CONCLUSION Our data demonstrates an inverse trend between TROY down-regulation and LGR5 up-regulation in GC tumors, as well as in response to H. pylori infection in mice. These findings support a potential negative modulatory role for TROY on LGR5 expression.
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MESH Headings
- Aged
- Animals
- Biomarkers, Tumor/analysis
- Biomarkers, Tumor/biosynthesis
- Biomarkers, Tumor/genetics
- Female
- Gene Expression Regulation, Neoplastic
- Helicobacter Infections/genetics
- Helicobacter Infections/metabolism
- Helicobacter Infections/pathology
- Humans
- Male
- Mice
- Middle Aged
- Receptors, G-Protein-Coupled/analysis
- Receptors, G-Protein-Coupled/biosynthesis
- Receptors, G-Protein-Coupled/genetics
- Receptors, Tumor Necrosis Factor/analysis
- Receptors, Tumor Necrosis Factor/biosynthesis
- Receptors, Tumor Necrosis Factor/genetics
- Stomach Neoplasms/genetics
- Stomach Neoplasms/metabolism
- Stomach Neoplasms/pathology
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Affiliation(s)
- Samaneh Saberi
- HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
| | - Abbas Piryaei
- Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
- Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
| | - Esmat Mirabzadeh
- Department of Molecular Medicine, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
| | - Maryam Esmaeili
- HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
| | - Toktam Karimi
- HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
| | - Sara Momtaz
- HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
| | - Afshin Abdirad
- Department of Pathology, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Niloofar Sodeifi
- Department of Andrology at Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
| | | | - Hossein Baharvand
- Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
| | - Marjan Mohammadi
- HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
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Rahman MM, Sarker MAK, Hossain MM, Alam MS, Islam MM, Shirin L, Sultana R, Sultana GNN. Association of p53 Gene Mutation With Helicobacter pylori Infection in Gastric Cancer Patients and Its Correlation With Clinicopathological and Environmental Factors. World J Oncol 2019; 10:46-54. [PMID: 30834051 PMCID: PMC6396778 DOI: 10.14740/wjon1087] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2019] [Accepted: 02/11/2019] [Indexed: 12/19/2022] Open
Abstract
BACKGROUND Gastric cancer is also a leading cancer in Bangladesh like that of the global incidences. It is speculated that environmental, bacterial infection and molecular factors might have been carrying the key role of rising trend of the disease. This study was aimed to investigate the association of mutated p53 gene with of Helicobacter pylori (H. pylori) infection, clinicopathological and some environmental factors of the gastric cancer patients. METHODS This cross-sectional study was carried out from January 2015 to December 2016 in a specialized cancer hospital of Bangladesh. Patients were selected randomly who were admitted for surgical intervention after diagnosis as adenocarcinoma of the stomach and physically fit for surgery. After admission proper evaluation of the patients was done. Tissue sample from the gastrectomy specimen along with the blood sample was sent to the related laboratories. After DNA extraction for p53, exons 5 and 6, they were adjusted for proper primer designing. Appropriate sequencing analysis of the result was done. Status of p53 was investigated to see their association with the result of the H. pylori, age and sex, tumor status, smoking and extra salt intake of the patients. Result of the study was calculated and analyzed by Chi-square and binomial logistic regression to find the association amongst them. RESULTS Among the 71 patients, mean age was 52.96 years old, male: female ratio were 48:23, age group above 41 years were 53 (74.6%), proliferative and ulceroproliferative group of the tumor dominated (87.3%). There were 52 cases with (73.2%) p53 mutation. Among the 51 H. pylori positive cases, 41 (80%) had p53 mutation (P = 0.033). Tumor size and lymph node status were found to be associated with the gene mutation (P = 0.05). Age also had strong correlation with the mutation (P = 0.015). Gene mutation was found mostly among the younger (≤ 40 years) group of patients (94.4%). Patient with extra salt intake was also found related with the mutation (P = 0.03). CONCLUSIONS Environmental and genetic factors seem to be risk factors for gastric cancer in Bangladesh. Nationwide anti H. pylori drive and further molecular research could elicit the other risk factors which might help to reduce the gastric cancer incidences in the country after taking appropriate measures.
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Affiliation(s)
- M. Mizanur Rahman
- Department of Surgical Oncology, National Institute of Cancer Research and Hospital, Mohakhali, Dhaka, Bangladesh
| | | | | | - Mohd. Sahajadul Alam
- National Institute of Cancer Research and Hospital, Mohakhali, Dhaka, Bangladesh
| | - Md. Monzurul Islam
- National Institute of Cancer Research and Hospital, Mohakhali, Dhaka, Bangladesh
| | - Laila Shirin
- National Institute of Cancer Research and Hospital, Mohakhali, Dhaka, Bangladesh
| | - Rokeya Sultana
- Centre for Advanced Research in Sciences (CARS), University of Dhaka, Dhaka, Bangladesh
| | - Gazi Nurun Nahar Sultana
- Genetic Engineering and Biotechnology Research Centre for Advanced Research in Sciences (CARS), University of Dhaka, Dhaka, Bangladesh
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Abuderman AA. Gastric cancer & prospects of cancer in Saudi Arabia peninsula. Saudi J Biol Sci 2018; 26:1095-1100. [PMID: 31516334 PMCID: PMC6734134 DOI: 10.1016/j.sjbs.2018.02.016] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/08/2018] [Revised: 02/04/2018] [Accepted: 02/25/2018] [Indexed: 12/13/2022] Open
Abstract
Gastric cancer is classified to be an aggressive disease with poor treatment outcome, as most cases remain undetected until later stages, wherein surgery and few chemotherapeutics become the only recommended treatment course. The process of cancer development is multistep involving many stages and types of precancerous lesions, and hence, routine monitoring becomes a necessity in those detected with these or exposed to risk factors. Studying the pattern of gastric cancer for any geographical region is also important to control mortality and focus on implementation of efficient management and treatment guidelines. The cause for gastric cancer can be genetic, racial as well as environmental, and hence the pattern of this malignancy differs across geographical regions and between the developing and the developed nations. In case of the Kindgom of Saudi Arabia, very few hospital-based reports have been published highlighting the pattern of gastric cancer, and the associated incidence and mortality rates. However, classified to be one of the most crucial cancer forms in Saudi Arabia, research pertaining to epidemiology, presentation and pathological features are limited. Studying gastric cancer occurrence from public health viewpoint is important also because eradication of causative agents like those that H. pylori has also shown been not reduce the risk of cancer development among individuals with atrophic metaplastic gastritis. In case of Saudi Arabia, many inherent risks for this malignancy exists like waterpipe smoking and shift in diet pattern from the traditional Mediterranean diet. Our review focusses on pattern of gastric cancer on a global scale in comparison to scenario in Saudi Arabia. The aim is to encompass all of the less stressed upon facts about this malignancy in the Kingdom, paving way for future work in this regards.
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Affiliation(s)
- Abdulwahab Ali Abuderman
- Basic Medical Science Department, College of Medicine, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia
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14
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Noto JM, Romero-Gallo J, Piazuelo MB, Peek RM. The Mongolian Gerbil: A Robust Model of Helicobacter pylori-Induced Gastric Inflammation and Cancer. Methods Mol Biol 2017; 1422:263-80. [PMID: 27246040 DOI: 10.1007/978-1-4939-3603-8_24] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
The Mongolian gerbil is an efficient, robust, and cost-effective rodent model that recapitulates many features of H. pylori-induced gastric inflammation and carcinogenesis in humans, allowing for targeted investigation of the bacterial determinants and environmental factors and, to a lesser degree, host constituents that govern H. pylori-mediated disease. This chapter discusses means through which the Mongolian gerbil model has been used to define mechanisms of H. pylori-inflammation and cancer as well as the current materials and methods for utilizing this model of microbially induced disease.
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Affiliation(s)
- Jennifer M Noto
- Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, 2215 Garland Avenue MRB IV 1030C, Nashville, TN, 37232-0252, USA
| | - Judith Romero-Gallo
- Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, 2215 Garland Avenue MRB IV 1030C, Nashville, TN, 37232-0252, USA
| | - M Blanca Piazuelo
- Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, 2215 Garland Avenue MRB IV 1030C, Nashville, TN, 37232-0252, USA
| | - Richard M Peek
- Division of Gastroenterology, Department of Medicine, Vanderbilt University Medical Center, 2215 Garland Avenue MRB IV 1030C, Nashville, TN, 37232-0252, USA.
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15
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Burkitt MD, Duckworth CA, Williams JM, Pritchard DM. Helicobacter pylori-induced gastric pathology: insights from in vivo and ex vivo models. Dis Model Mech 2017; 10:89-104. [PMID: 28151409 PMCID: PMC5312008 DOI: 10.1242/dmm.027649] [Citation(s) in RCA: 80] [Impact Index Per Article: 10.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
Gastric colonization with Helicobacter pylori induces diverse human pathological conditions, including superficial gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma and its precursors. The treatment of these conditions often relies on the eradication of H. pylori, an intervention that is increasingly difficult to achieve and that does not prevent disease progression in some contexts. There is, therefore, a pressing need to develop new experimental models of H. pylori-associated gastric pathology to support novel drug development in this field. Here, we review the current status of in vivo and ex vivo models of gastric H. pylori colonization, and of Helicobacter-induced gastric pathology, focusing on models of gastric pathology induced by H. pylori, Helicobacter felis and Helicobacter suis in rodents and large animals. We also discuss the more recent development of gastric organoid cultures from murine and human gastric tissue, as well as from human pluripotent stem cells, and the outcomes of H. pylori infection in these systems.
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Affiliation(s)
- Michael D Burkitt
- Gastroenterology Research Unit, Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, UK
| | - Carrie A Duckworth
- Gastroenterology Research Unit, Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, UK
| | - Jonathan M Williams
- Pathology and Pathogen Biology, Royal Veterinary College, North Mymms AL9 7TA, UK
| | - D Mark Pritchard
- Gastroenterology Research Unit, Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, UK
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16
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Zaidi SF, Ahmed K, Saeed SA, Khan U, Sugiyama T. Can Diet Modulate Helicobacter pylori-associated Gastric Pathogenesis? An Evidence-Based Analysis. Nutr Cancer 2017; 69:979-989. [PMID: 28937799 DOI: 10.1080/01635581.2017.1359310] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
Helicobacter pylori is involved in the pathogenesis of gastritis, peptic ulcer, and gastric cancer. The infection is prevalent in more than half of the world's population. Although the infection may lead to detrimental consequences, still the majority of the infected individuals only develop mild gastritis. Several factors are behind this paradoxical outcome including virulence of the infecting H. pylori strains, genetic background of the host, and factors related to lifestyle such as dietary habits. Among these, lifestyle including dietary factors was not in the limelight, until recently, as one of the important factors that could modulate H. pylori-linked gastric diseases. This review is directed to gather and elucidate the role of dietary components in augmenting or attenuating pathological processes initiated by H. pylori. Available evidence strongly supports the notion that the diet may play a critical role in defining the final outcome of H. pylori infection particularly if certain dietary components are taken on a regular basis for a long time. Despite a recent surge in research related to the role of dietary ingredients, further studies involving large-scale clinical trials are required to gain a better understanding of the precise role played by the dietary ingredients in H. pylori-associated pathogenesis.
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Affiliation(s)
- Syed Faisal Zaidi
- a Department of Basic Medical Sciences, College of Medicine , King Saud bin Abdulaziz University of Health Sciences , Jeddah , Kingdom of Saudi Arabia
| | - Kanwal Ahmed
- a Department of Basic Medical Sciences, College of Medicine , King Saud bin Abdulaziz University of Health Sciences , Jeddah , Kingdom of Saudi Arabia
| | - Sheikh Abdul Saeed
- a Department of Basic Medical Sciences, College of Medicine , King Saud bin Abdulaziz University of Health Sciences , Jeddah , Kingdom of Saudi Arabia
| | - Usmanghani Khan
- b Faculty of Pharmacy , Jinnah University for Women , Karachi , Pakistan
| | - Toshiro Sugiyama
- c Department of Gastroenterology, Faculty of Medicine , University of Toyama , Toyama , Japan
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17
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Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond. Int J Mol Sci 2017; 18:ijms18081699. [PMID: 28771198 PMCID: PMC5578089 DOI: 10.3390/ijms18081699] [Citation(s) in RCA: 43] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/17/2017] [Revised: 07/31/2017] [Accepted: 07/31/2017] [Indexed: 12/15/2022] Open
Abstract
Although its prevalence is declining, gastric cancer remains a significant public health issue. The bacterium Helicobacter pylori is known to colonize the human stomach and induce chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Results using a Mongolian gerbil model revealed that H. pylori infection increased the incidence of carcinogen-induced adenocarcinoma, whereas curative treatment of H. pylori significantly lowered cancer incidence. Furthermore, some epidemiological studies have shown that eradication of H. pylori reduces the development of metachronous cancer in humans. However, other reports have warned that human cases of atrophic metaplastic gastritis are already at risk for gastric cancer development, even after eradication of these bacteria. In this article, we discuss the effectiveness of H. pylori eradication and the morphological changes that occur in gastric dysplasia/cancer lesions. We further assess the control of gastric cancer using various chemopreventive agents.
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18
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Lu D, Pan C, Ye C, Duan H, Xu F, Yin L, Tian W, Zhang S. Meta-analysis of Soy Consumption and Gastrointestinal Cancer Risk. Sci Rep 2017; 7:4048. [PMID: 28642459 PMCID: PMC5481399 DOI: 10.1038/s41598-017-03692-y] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/29/2016] [Accepted: 05/15/2017] [Indexed: 12/13/2022] Open
Abstract
Soy consumption has received considerable attention for its potential role in reducing cancer incidence and mortality. However, its effects on gastrointestinal (GI) cancer are controversial. Therefore, we performed a meta-analysis to evaluate the association between soy consumption and gastrointestinal cancer risk by searching for prospective studies in PubMed, Web of Science, EMBASE and the reference lists of the included articles. The study-specific odds ratio (OR), relative risk (RR) or hazard ratio (HR) estimates and 95% confidence intervals (CIs) were pooled using either a fixed-effect or random-effect model. Twenty-two independent prospective studies were eligible for our meta-analysis, including 21 cohort studies and one nested case-control study. Soy product consumption was inversely associated with the incidence of overall GI cancer (0.857; 95% CI: 0.766, 0.959) and the gastric cancer subgroup (0.847; 95% CI: 0.722, 0.994) but not the colorectal cancer subgroup. After stratifying the results according to gender, an inverse association was observed between soy product intake and the incidence of GI cancer for females (0.711; 95% CI: 0.506, 0.999) but not for males.
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Affiliation(s)
- Demin Lu
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
- Department of Medical Oncology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Chi Pan
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Chenyang Ye
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Huijie Duan
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Fei Xu
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Li Yin
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Wei Tian
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Suzhan Zhang
- Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
- Reseach Center for Air Pollution and Health, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310009, China.
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19
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The effect of trimethylamine N-oxide on Helicobacter pylori-induced changes of immunoinflammatory genes expression in gastric epithelial cells. Int Immunopharmacol 2017; 43:172-178. [DOI: 10.1016/j.intimp.2016.11.032] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2016] [Revised: 11/26/2016] [Accepted: 11/28/2016] [Indexed: 01/30/2023]
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20
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Zaidi SF. Helicobacter pylori associated Asian enigma: Does diet deserve distinction? World J Gastrointest Oncol 2016; 8:341-350. [PMID: 27096029 PMCID: PMC4824712 DOI: 10.4251/wjgo.v8.i4.341] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/14/2015] [Revised: 11/23/2015] [Accepted: 01/22/2016] [Indexed: 02/05/2023] Open
Abstract
Helicobacter pylori (H. pylori) is one of the most widespread infections in humans worldwide that chronically infects up to 50% of the world’s population. The infection is involved in the pathogenesis of chronic active gastritis, peptic ulcer, mucosa-associated lymphoid tissue lymphoma and gastric cancer, therefore, it has been classified as class I definite carcinogen by the World Health Organization. Despite the established etiological role of H. pylori, its actual distribution and association with related diseases is controversial and there is a large intercountry variation especially among Asian countries. H. pylori infection is more frequent in developing countries like India, Pakistan, and Bangladesh as compared to developed Asian countries like Japan, China and South Korea. However, the frequency of gastric cancer is comparatively lower in India, Pakistan, and Bangladesh with that of Japan, China and South Korea. Such phenomenon of clinical diversity, defined as enigma, is judged by genetic variability of the infecting H. pylori strains, differences in the host genetic background in various ethnic groups, and environmental factors such as dietary habits. Most of the studies have so far focused on the bacterial factor while environmental issues, including dietary components, were not given due attention as one of the factors related with H. pylori associated gastric carcinogenesis. The dietary factor has been suggested to play an important role in H. pylori related carcinogenesis, and in this respect several studies have corroborated the intake of various dietary components as modulatory factors for gastric cancer risk. In this review, such studies, from in vitro experiments to clinical trials, are being focused in detail with respect to enigma associated with H. pylori. It may be conceivably concluded from the available evidence that dietary factor can be a game changer in the scenario of Asian enigma, particularly in high risk population infected with virulent H. pylori strains, however further affirmation studies are desperately needed to achieve conclusive outcomes.
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Khatoon J, Rai RP, Prasad KN. Role of Helicobacter pylori in gastric cancer: Updates. World J Gastrointest Oncol 2016; 8:147-158. [PMID: 26909129 PMCID: PMC4753165 DOI: 10.4251/wjgo.v8.i2.147] [Citation(s) in RCA: 78] [Impact Index Per Article: 8.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2015] [Revised: 07/14/2015] [Accepted: 12/15/2015] [Indexed: 02/05/2023] Open
Abstract
Helicobacter pylori (H. pylori) infection is highly prevalent in human, affecting nearly half of the world’s population; however, infection remains asymptomatic in majority of population. During its co-existence with humans, H. pylori has evolved various strategies to maintain a mild gastritis and limit the immune response of host. On the other side, presence of H. pylori is also associated with increased risk for the development of various gastric pathologies including gastric cancer (GC). A complex combination of host genetics, environmental agents, and bacterial virulence factors are considered to determine the susceptibility as well as the severity of outcome in a subset of individuals. GC is one of the most common cancers and considered as the third most common cause of cancer related death worldwide. Many studies had proved H. pylori as an important risk factor in the development of non-cardia GC. Although both H. pylori infection and GC are showing decreasing trends in the developed world, they still remain a major threat to human population in the developing countries. The current review attempts to highlight recent progress in the field of research on H. pylori induced GC and aims to provide brief insight into H. pylori pathogenesis, the role of major virulence factors of H. pylori that modulates the host environment and transform the normal gastric epithelium to neoplastic one. This review also emphasizes on the mechanistic understanding of how colonization and various virulence attributes of H. pylori as well as the host innate and adaptive immune responses modulate the diverse signaling pathways that leads to different disease outcomes including GC.
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22
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Amieva M, Peek RM. Pathobiology of Helicobacter pylori-Induced Gastric Cancer. Gastroenterology 2016; 150:64-78. [PMID: 26385073 PMCID: PMC4691563 DOI: 10.1053/j.gastro.2015.09.004] [Citation(s) in RCA: 625] [Impact Index Per Article: 69.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/07/2015] [Revised: 09/01/2015] [Accepted: 09/03/2015] [Indexed: 02/07/2023]
Abstract
Colonization of the human stomach by Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of a complex relationship among human cells, microbes, and their environment. It is also a puzzle of enormous medical importance given the incidence and lethality of gastric cancer worldwide. We review recent findings that have changed how we view these relationships and affected the direction of gastric cancer research. For example, recent data have indicated that subtle mismatches between host and microbe genetic traits greatly affect the risk of gastric cancer. The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activate properties of stemness show the sophisticated relationship between H pylori and progenitor cells in the gastric mucosa. The observation that cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem cells supports these observations. The ability to mimic these interactions in human gastric organoid cultures as well as animal models will allow investigators to more fully unravel the extent of H pylori control on the renewing gastric epithelium. Finally, our realization that external environmental factors, such as dietary components and essential micronutrients, as well as the gastrointestinal microbiota, can change the balance between H pylori's activity as a commensal or a pathogen has provided direction to studies aimed at defining the full carcinogenic potential of this organism.
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Affiliation(s)
- Manuel Amieva
- Department of Microbiology and Immunology, Stanford University, Palo Alto, California; Department of Pediatrics, Stanford University, Palo Alto, California
| | - Richard M Peek
- Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee.
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23
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Solnick JV, Eaton KA, Peek RM. Animal Models of Helicobacter pylori Infection. HELICOBACTER PYLORI RESEARCH 2016:273-297. [DOI: 10.1007/978-4-431-55936-8_11] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/02/2025]
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24
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Shin JY, Kim J, Choi KS, Suh M, Park B, Jun JK. Relationship between Salt Preference and Gastric Cancer Screening: An Analysis of a Nationwide Survey in Korea. Cancer Res Treat 2015; 48:1037-44. [PMID: 26693914 PMCID: PMC4946365 DOI: 10.4143/crt.2015.333] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2015] [Accepted: 11/16/2015] [Indexed: 12/14/2022] Open
Abstract
Purpose Epidemiological studies have demonstrated an association between excessive salt intake and gastric cancer risk, and this potential risk increases the need for adequate gastric cancer screening in individuals with high salt intake. However, the association between salt intake and gastric cancer screening in the general population has rarely been investigated. We explored the association between salt preference and participation in gastric cancer screening among a nationally representative Korean population. Materials and Methods The study population was derived from the Korean National Cancer Screening Survey (KNCSS) 2006-2007, an annual nationwide interview survey investigating cancer screening rates. Of 4,055 individuals who participated in the KNCSS 2006-2007, 3,336 individuals aged over 40 years were included in our analysis. The odds ratio (OR) and 95% confidence interval (CI) were estimated using polytomous logistic regression. Results Individuals with higher salt preference were less likely to participate in regular gastric cancer screening. After adjusting for age, sex, monthly household income, education, family history of cancer, and self-rated health status, ORs for undergoing regular gastric cancer screening were 1.00, 0.82 (95% CI, 0.61 to 1.12), 0.74 (95% CI, 0.54 to 1.00), 0.77 (95% CI, 0.56 to 1.05), and 0.38 (95% CI, 0.16 to 0.92) according to the level of salt preference (p for trend=0.048). Conclusion Individuals with higher salt preference showed suboptimal gastric cancer screening adherence compared to those with a lower salt preference. These findings highlight the need for better delivery of educational messages to change risk perceptions regarding gastric cancer screening practice.
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Affiliation(s)
- Ji-Yeon Shin
- Department of Preventive Medicine, Eulji University School of Medicine, Daejeon, Korea
| | - Jeongseon Kim
- Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Korea
| | - Kui Son Choi
- Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Korea.,National Cancer Control Institute, National Cancer Center, Goyang, Korea
| | - Mina Suh
- National Cancer Control Institute, National Cancer Center, Goyang, Korea
| | - Boyoung Park
- Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Korea.,National Cancer Control Institute, National Cancer Center, Goyang, Korea
| | - Jae Kwan Jun
- Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Korea.,National Cancer Control Institute, National Cancer Center, Goyang, Korea
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25
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Umesawa M, Iso H, Fujino Y, Kikuchi S, Tamakoshi A. Salty Food Preference and Intake and Risk of Gastric Cancer: The JACC Study. J Epidemiol 2015; 26:92-7. [PMID: 26477994 PMCID: PMC4728120 DOI: 10.2188/jea.je20150023] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
Background High sodium intake is a potential risk factor of gastric cancer. However, limited information is available on the relationship between salty food preference or intake and risk of gastric cancer. The aim of the present study was to determine the association between these variables among the Japanese population. Methods Between 1988 and 1990, 15 732 men and 24 997 women aged 40–79 years old with no history of cancer or cardiovascular disease completed a lifestyle questionnaire that included information about food intake. The subjects were enrolled in the Japan Collaborative Cohort (JACC) Study for Evaluation of Cancer Risk Sponsored by Monbusho. After a median follow-up of 14.3 years, 787 incident gastric cancers were documented. We examined the associations between salty food preference and intake and gastric cancer incidence using the Cox proportional hazard model. Results The risk of gastric cancer among subjects with a strong preference for salty food was approximately 30% higher than among those who preferred normal-level salty food (hazard ratio [HR] 1.31; 95% confidence interval [CI], 1.02–1.67). The risk of gastric cancer in subjects who consumed 3 and ≥4 bowls/day of miso soup was approximately 60% higher than in those who consumed less miso soup (HR 1.67; 95% CI, 1.16–2.39 and HR 1.64; 95% CI, 1.11–2.42, respectively). Sodium intake correlated positively and linearly with risk of gastric cancer (P for trend = 0.002). Conclusions The present study showed that salty food preference, consumption of large quantities of miso soup, and high sodium intake were associated with increased risk of gastric cancer among Japanese people.
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Affiliation(s)
- Mitsumasa Umesawa
- Department of Public Health, Dokkyo Medical University School of Medicine
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26
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Fock KM. Review article: the epidemiology and prevention of gastric cancer. Aliment Pharmacol Ther 2014; 40:250-60. [PMID: 24912650 DOI: 10.1111/apt.12814] [Citation(s) in RCA: 305] [Impact Index Per Article: 27.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/16/2013] [Revised: 11/01/2013] [Accepted: 05/12/2014] [Indexed: 12/12/2022]
Abstract
BACKGROUND Gastric cancer can be divided into cardia and noncardia gastric adenocarcinoma (NCGA). Non cardia gastric cancer is a disease that has declined in global incidence but has remained as an extremely lethal cancer. AIM To review recent advances in epidemiology and strategies in prevention of non cardia gastric cancer. METHODS A rapid literature search strategy was developed for all English language literature published before March 2013. The search was conducted using the electronic databases PubMed and EMBASE. The search strategy included the keywords 'stomach neoplasms', 'gastric cancer', 'epidemiology', 'risk factor', 'early detection of cancer', 'mass screening', 'cancer burden', 'prevention' and 'cost-effectiveness'. The search strategy was adjusted according to different requirements for each database. The specific search was also performed in cancer-related websites for country-specific information. The search was limited to past 10 years. RESULTS Gastric cancer is the fifth most common cancer but the third leading cause of cancer death. The case fatality rate is 75%. Screening by radiological or endoscopic methods has limited success in prevention of gastric cancer. Helicobacter pylori has been identified as a carcinogen, accounting for 60-70% of gastric cancer globally and eradication is a potential preventive measure. A meta-analysis in 2009 demonstrated that individuals treated with H. pylori eradication therapy can reduce gastric cancer risk. The extended Shandong Intervention trial that lasted 14.3 years showed that H. pylori eradication therapy significantly reduced gastric cancer incidence by 39%. Consensus groups from Asia, Europe and Japan have recommended H. pylori eradication as primary prevention in high-risk areas. Following eradication therapy, endoscopic surveillance of pre-malignant lesions using enhanced imaging appears to be another promising preventive strategy. CONCLUSIONS Gastric cancer remains a major diagnostic and therapeutic challenge. There is emerging evidence that H. pylori eradication in high gastric cancer regions can lead to a decline in the incidence of this highly lethal disease.
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Affiliation(s)
- K M Fock
- Changi General Hospital, Singapore
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Epplein M, Zheng W, Li H, Peek RM, Correa P, Gao J, Michel A, Pawlita M, Cai Q, Xiang YB, Shu XO. Diet, Helicobacter pylori strain-specific infection, and gastric cancer risk among Chinese men. Nutr Cancer 2014; 66:550-7. [PMID: 24666234 DOI: 10.1080/01635581.2014.894096] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Evidence for the association of diet and gastric cancer is equivocal, and the majority of previous studies have not evaluated the interaction of diet and infection with Helicobacter pylori, the leading risk factor for gastric cancer. We examined these associations among 226 cases and 451 controls nested within a prospective cohort. Dietary intakes were calculated from validated food frequency questionnaires. Blood levels of 15 antibodies to Helicobacter pylori proteins were assessed using multiplex serology. Odds ratios (ORs) were calculated using logistic regression. Among individuals infected with high-risk Helicobacter pylori (sero-positivity to 5-6 virulent H. pylori proteins), increasing intake of red meat, heme iron, and sodium increased risk (comparing highest tertile to lowest: ORs [95% confidence interval {CI}]: 1.85 [1.01-3.40]; 1.95 [1.06-3.57]; and 1.76 [0.91-3.43], respectively) while increasing intake of fruit decreased gastric cancer risk (comparing highest tertile of intake to lowest: OR [95% CI]: 0.52 [0.28-0.94]). No associations of diet with risk were found among individuals infected with low-risk H. pylori (P for interaction for red meat and sodium: 0.02 and 0.01, respectively). In this population with over 90% prevalence of CagA-positive H. pylori infection, categorizing individuals using H. pylori multiplex serology may identify individuals for whom a diet intervention may be effective.
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Affiliation(s)
- Meira Epplein
- a Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt-Ingram Cancer Center , Vanderbilt University School of Medicine , Nashville , Tennessee , USA
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28
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Abstract
Since its discovery in 1982, the global importance of Helicobacter pylori-induced disease, particularly in developing countries, remains high. The use of rodent models, particularly mice, and the unanticipated usefulness of the gerbil to study H. pylori pathogenesis have been used extensively to study the interactions of the host, the pathogen, and the environmental conditions influencing the outcome of persistent H. pylori infection. Dietary factors in humans are increasingly recognized as being important factors in modulating progression and severity of H. pylori-induced gastric cancer. Studies using rodent models to verify and help explain mechanisms whereby various dietary ingredients impact disease outcome should continue to be extremely productive.
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Affiliation(s)
- James G. Fox
- Division of Comparative Medicine, Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts
| | - Timothy C. Wang
- Division of Digestive and Liver Diseases, Department of Medicine, Columbia University Medical Center, New York, New York
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29
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Abstract
Humans began to use large amounts of salt for the main purpose of food preservation approximately 5,000 years ago and, although since then advanced technologies have been developed allowing drastic reduction in the use of salt for food storage, excess dietary salt intake remains very common. Gastric cancer is a common neoplasia, and dietary factors, including salt consumption, are considered relevant to its causation. A number of experimental studies supported the cocarcinogenic effect of salt through synergic action with Helicobacter pylori infection, in addition to some independent effects such as increase in the rate of cell proliferation and of endogenous mutations. Many epidemiological studies analyzed the relationship between excess salt intake and risk of gastric cancer. Both cross-sectional and prospective studies indicated a possibly dose-dependent positive association. In particular, a comprehensive meta-analysis of longitudinal studies detected a strong adverse effect of total salt intake and salt-rich foods on the risk of gastric cancer in the general population. Altogether, the epidemiological, clinical, and experimental evidence supports the possibility of a substantial reduction in the rates of gastric cancer through progressive reduction in population salt intake.
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Affiliation(s)
- Lanfranco D'Elia
- Department of Clinical and Experimental Medicine, "Federico II" University of Naples, Naples, Italy
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30
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Abstract
Gastric adenocarcinoma is a leading cause of cancer-related death worldwide, and Helicobacter pylori infection is one of the strongest known risk factors for this malignancy. H. pylori strains exhibit a high level of genetic diversity, and the risk of gastric cancer is higher in persons carrying certain strain types (for example, those that contain a cag pathogenicity island or type s1 vacA alleles) than in persons carrying other strain types. Additional risk factors for gastric cancer include specific human genetic polymorphisms and specific dietary preferences (for example, a high-salt diet or a diet deficient in fruits and vegetables). Finally, iron-deficiency anemia is a risk factor for gastric cancer. Recent studies have provided evidence that several dietary risk factors for gastric cancer directly impact H. pylori virulence. In this review article, we discuss mechanisms by which diet can modulate H. pylori virulence and thereby influence gastric cancer risk.
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Affiliation(s)
- Timothy L Cover
- Division of Infectious Diseases; Vanderbilt University School of Medicine; Nashville, TN USA,Department of Pathology, Microbiology, and Immunology; Vanderbilt University School of Medicine; Nashville, TN USA,Veterans Affairs Tennessee Valley Healthcare System; Nashville, TN USA
| | - Richard M Peek, Jr
- Division of Gastroenterology, Department of Medicine; Vanderbilt University School of Medicine; Nashville, TN USA,Correspondence to: Richard M Peek, Jr,
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31
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Yoshida T, Kato J, Inoue I, Yoshimura N, Deguchi H, Mukoubayashi C, Oka M, Watanabe M, Enomoto S, Niwa T, Maekita T, Iguchi M, Tamai H, Utsunomiya H, Yamamichi N, Fujishiro M, Iwane M, Takeshita T, Ushijima T, Ichinose M. Cancer development based on chronic active gastritis and resulting gastric atrophy as assessed by serum levels of pepsinogen and Helicobacter pylori antibody titer. Int J Cancer 2013; 134:1445-57. [PMID: 24009139 DOI: 10.1002/ijc.28470] [Citation(s) in RCA: 115] [Impact Index Per Article: 9.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/09/2013] [Accepted: 08/22/2013] [Indexed: 12/11/2022]
Abstract
Our study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or the resulting chronic atrophic gastritis (CAG). A cohort of 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) and H. pylori antibody titer had been measured to assess the activity and stage of H. pylori-associated chronic gastritis, was followed for up to 16 years, and cancer development was investigated. In subjects with a serologically diagnosed healthy stomach (H. pylori-negative/CAG-negative), cancer incidence rate was low, at 16/100,000 person-years. With the establishment of H. pylori infection and progression of chronic gastritis, significant stepwise cancer risk elevations were seen from CAG-free subjects (H. pylori-positive/CAG-negative) [hazard ratio (HR) = 8.9, 95% confidence interval (CI) = 2.7-54.7] to subjects with CAG (H. pylori-positive/CAG-positive) (HR = 17.7, 95% CI = 5.4-108.6) and finally to subjects with metaplastic gastritis (H. pylori-negative/CAG-positive) (HR = 69.7, 95% CI = 13.6-502.9). In H. pylori-infected CAG-free subjects, significantly elevated cancer risk was observed in the subgroup with active inflammation-based high PG II level or potent immune response-based high H. pylori antibody titer; the former was associated with a particularly high risk of diffuse-type cancer, and both subgroups showed high cancer incidence rates of around 250/100,000 person-years, comparable to that in subjects with CAG. No such risk elevation was observed in H. pylori-infected subjects with CAG. These results clearly indicate that gastric cancer develops mainly from the gastritis-atrophy-metaplasia-cancer sequence and partly from active inflammation-based direct carcinogenesis, and that serum levels of PG and H. pylori antibody titer provide indices of cancer development in H. pylori-infected subjects.
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Affiliation(s)
- Takeichi Yoshida
- Second Department of Internal Medicine, School of Medicine, Wakayama Medical University, Wakayama City, Wakayama, Japan
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32
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Toyoda T, Tsukamoto T, Yamamoto M, Ban H, Saito N, Takasu S, Shi L, Saito A, Ito S, Yamamura Y, Nishikawa A, Ogawa K, Tanaka T, Tatematsu M. Gene expression analysis of a Helicobacter pylori-infected and high-salt diet-treated mouse gastric tumor model: identification of CD177 as a novel prognostic factor in patients with gastric cancer. BMC Gastroenterol 2013; 13:122. [PMID: 23899160 PMCID: PMC3734037 DOI: 10.1186/1471-230x-13-122] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/26/2012] [Accepted: 07/22/2013] [Indexed: 12/13/2022] Open
Abstract
BACKGROUND Helicobacter pylori (H. pylori) infection and excessive salt intake are known as important risk factors for stomach cancer in humans. However, interactions of these two factors with gene expression profiles during gastric carcinogenesis remain unclear. In the present study, we investigated the global gene expression associated with stomach carcinogenesis and prognosis of human gastric cancer using a mouse model. METHODS To find candidate genes involved in stomach carcinogenesis, we firstly constructed a carcinogen-induced mouse gastric tumor model combined with H. pylori infection and high-salt diet. C57BL/6J mice were given N-methyl-N-nitrosourea in their drinking water and sacrificed after 40 weeks. Animals of a combination group were inoculated with H. pylori and fed a high-salt diet. Gene expression profiles in glandular stomach of the mice were investigated by oligonucleotide microarray. Second, we examined an availability of the candidate gene as prognostic factor for human patients. Immunohistochemical analysis of CD177, one of the up-regulated genes, was performed in human advanced gastric cancer specimens to evaluate the association with prognosis. RESULTS The multiplicity of gastric tumor in carcinogen-treated mice was significantly increased by combination of H. pylori infection and high-salt diet. In the microarray analysis, 35 and 31 more than two-fold up-regulated and down-regulated genes, respectively, were detected in the H. pylori-infection and high-salt diet combined group compared with the other groups. Quantitative RT-PCR confirmed significant over-expression of two candidate genes including Cd177 and Reg3g. On immunohistochemical analysis of CD177 in human advanced gastric cancer specimens, over-expression was evident in 33 (60.0%) of 55 cases, significantly correlating with a favorable prognosis (P = 0.0294). Multivariate analysis including clinicopathological factors as covariates revealed high expression of CD177 to be an independent prognostic factor for overall survival. CONCLUSIONS These results suggest that our mouse model combined with H. pylori infection and high-salt diet is useful for gene expression profiling in gastric carcinogenesis, providing evidence that CD177 is a novel prognostic factor for stomach cancer. This is the first report showing a prognostic correlation between CD177 expression and solid tumor behavior.
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33
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Zhong C, Li KN, Bi JW, Wang BC. Sodium intake, salt taste and gastric cancer risk according to Helicobacter pylori infection, smoking, histological type and tumor site in China. Asian Pac J Cancer Prev 2013; 13:2481-4. [PMID: 22938408 DOI: 10.7314/apjcp.2012.13.6.2481] [Citation(s) in RCA: 37] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
AIM The risk factors mostly strongly associated with gastric cancer are gastric bacteria Helicobacter pylori and diet. Using a case-control study among residents in Jinan, we examined the association between the salt taste and gastric cancer according to H. pylori infection, smoking and histological type as well as tumor site. METHODS This population-based case-control study included 207 cases and 410 controls. Data on potential risk factors of gastric cancer were obtained by interview of cases and controls with a questionnaire, salt taste preference was measured for all subjects, and IgG antibodies to H. pylori were applied to assess infection. Risk measures were determined using unconditional logistic regression. RESULTS The proportions of salt taste at intervals of 1.8-7.2 g/L and ≥ 7.2 g/L were significantly higher in cases than controls, with ORs of 1.56 (1.23-3.64) and 2.03 (2.12- 4.11), respectively, subjects with high salt intake having an elevated risk for gastric cancer when infected with H. pylori. Significant modification by smoking and tumor site was observed across the different measures of salt intake, the highest salt taste showed higher cancer risk in ever smokers or with non-cardia cancers. CONCLUSION Our study supports the view that high intake of sodium is an important dietary risk factor for gastric cancer, with a synergistic effect found between salt and H.pylori and smoking, dependent on the tumor site.
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Affiliation(s)
- Chen Zhong
- Department of oncology, General Hospital of Jinan Military Region, Jinan, China
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34
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Up-regulation of neutrophil activating protein in Helicobacter pylori under high-salt stress: structural and phylogenetic comparison with bacterial iron-binding ferritins. Biochimie 2013; 95:1136-45. [PMID: 23352965 DOI: 10.1016/j.biochi.2012.12.017] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2012] [Accepted: 12/30/2012] [Indexed: 02/08/2023]
Abstract
It is generally accepted that most gastrointestinal diseases are probably caused by the bacterial pathogen Helicobacter pylori (H. pylori). In this study we have focused on the comparison of protein expression profiles of H. pylori grown under normal and high-salt conditions by a proteomics approach. We have identified about 190 proteins whose expression levels changed after growth at high salt concentration. Among these proteins, neutrophil-activating protein (NapA) was found to be consistently up-regulated under osmotic stress brought by high salts. We have investigated the effect of high salt on secondary and tertiary structures of NapA by circular dichroism spectroscopy followed by analytical ultracentrifugation to monitor the change of quaternary structure of recombinant NapA with increasing salt concentration. The loss of iron-binding activity of NapA coupled with noticeable energetic variation in protein association of NapA as revealed by isothermal titration calorimetry was found under high salt condition. The phylogenetic tree analysis based on sequence comparison of 16 protein sequences encompassing NapA proteins and ferritin of H. pylori and other prokaryotic organisms pointed to the fact that all H. pylori NapA proteins of human origin are more homologous to NapA of Helicobacter genus than to other bacterial NapA. Based on computer modeling, NapA proteins from H. pylori of human isolates are found more similar to ferritin from H. pylori than to NapA from other species of bacteria. Taken together, these results suggested that divergent evolution of NapA and ferritin possessing dissimilar and diverse sequences follows a path distinct from that of convergent evolution of NapA and ferritin with similar dual functionality of iron-binding and ferroxidase activities.
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35
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Helicobacter pylori infection and gastric carcinogenesis in rodent models. Semin Immunopathol 2012; 35:177-90. [PMID: 23111700 DOI: 10.1007/s00281-012-0357-1] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/24/2012] [Accepted: 10/15/2012] [Indexed: 02/07/2023]
Abstract
Helicobacter pylori infection is an important factor for gastric carcinogenesis in human. In carcinogen-treated Mongolian gerbils, H. pylori infection enhances stomach carcinogenesis, while infection alone induced severe hyperplasia called heterotopic proliferative glands. A high-salt diet or early acquisition of the bacteria exacerbates inflammation and carcinogenesis. Oxygen radical scavengers or anti-inflammatory chemicals as well as eradication of H. pylori are effective to prevent carcinogenesis. H. pylori-associated inflammation induces intestinal metaplasia and intestinalization of stomach cancers independently. It is necessary to control cancer development not only in H. pylori-positive cases but also in H. pylori-negative metaplastic gastritis.
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36
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Nanjo S, Asada K, Yamashita S, Nakajima T, Nakazawa K, Maekita T, Ichinose M, Sugiyama T, Ushijima T. Identification of gastric cancer risk markers that are informative in individuals with past H. pylori infection. Gastric Cancer 2012; 15:382-8. [PMID: 22237657 DOI: 10.1007/s10120-011-0126-1] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/25/2011] [Accepted: 11/26/2011] [Indexed: 02/07/2023]
Abstract
BACKGROUND Epigenomic damage induced by Helicobacter pylori infection is accumulated in gastric mucosae before the development of malignancy. In individuals without current H. pylori infection, DNA methylation levels of specific CpG islands (CGIs) are associated with gastric cancer risk. Because risk estimation in individuals with past infection is clinically important, we here aimed to identify the risk markers that reflect epigenomic damage induced by H. pylori infection, and that are informative in these individuals. METHODS Gastric mucosae were obtained from 55 gastric cancer patients (GC-Pt) (21 with current infection and 34 with past infection) and 55 healthy volunteers (HV) (7 never-infected, 21 with current infection, and 27 with past infection). Hypermethylated CGIs were searched for by methylated DNA immunoprecipitation-CGI microarray, and methylation levels were analyzed by quantitative methylation-specific polymerase chain reaction (PCR). RESULTS By microarray analysis of a pool of three samples from GC-Pt with past infection and another pool of samples from HV with past infection, 15 hypermethylated CGIs in the former pool were isolated. Seven of them had significantly higher methylation levels in GC-Pt with past infection (n = 10) than in HV with past infection (n = 10) (P < 0.001). In a validation cohort (21 GC-Pt with past infection and 14 HV with past infection), the seven new markers had large areas under the receiver-operating characteristic curves (0.78-0.84) and high odds ratios (12.7-36.0) compared with two currently available markers (0.60-0.65, 5.0-5.7). CONCLUSIONS We identified seven novel gastric cancer risk markers that are highly informative in individuals with past infection.
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Affiliation(s)
- Sohachi Nanjo
- Division of Epigenomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
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37
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Howlett M, Chalinor HV, Buzzelli JN, Nguyen N, van Driel IR, Bell KM, Fox JG, Dimitriadis E, Menheniott TR, Giraud AS, Judd LM. IL-11 is a parietal cell cytokine that induces atrophic gastritis. Gut 2012; 61:1398-409. [PMID: 22180059 PMCID: PMC3471558 DOI: 10.1136/gutjnl-2011-300539] [Citation(s) in RCA: 48] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND AND AIMS IL-is important in gastric damage, mucosal repair and gastric cancer progression. We analysed IL-11 expression in H.pylori infected mouse stomach, the site of gastric IL-11 expression in mice and humans, and the effect of exogenous IL-11 on gastric mucosal homeostasis. METHODS IL-11 protein was localised in mouse and human stomach. The impact of chronic, exogenous IL-11 on normal mouse stomach was examined histologically and transcriptionally by microarray, confirmed by mRNA and protein analysis. Functional impact of IL-11 on gastric acid secretion was determined. RESULTS In mice infected with H.pylori, IL-11 was increased in fundic mucosa with temporal expression similar to IL-1b. IL-11 protein was localised predominantly to parietal cells in mouse and human stomach. Application of exogenous IL-11 to resulted in fundic parietal and chief cell loss, hyperplasia, mucous cell metaplasia and inflammation. Coincident with cellular changes were an increased gastric pH, altered parietal cell ultrastructure and altered gene expression, particularly genes involved in immune response and ion transport which could result in compromised acid secretion. We confirmed that a single dose of IL-11 effectively ablated the gastric response to histamine. CONCLUSIONS IL-11 is a parietal cell cytokine that blocks gastric acid secretion, likely via reducing expression of parietal cell ion transport genes, CCKb and histamine H2 receptors. IL-11 expression is increased in H. pylori infected mouse stomach and treatment of wild type mice with IL-11 induced changes in the gastric fundic mucosa reminiscent of chronic atrophic gastritis, a precursor to gastric cancer.
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Affiliation(s)
- Meegan Howlett
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
| | - Heather V Chalinor
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
| | - Jon N Buzzelli
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
| | - Nhung Nguyen
- Department of Biochemistry and Molecular Biology, Bio 21 Molecular Sciences and Biotechnology Institute, University of Melbourne, Parkville, Victoria, Australia
| | - Ian R van Driel
- Department of Biochemistry and Molecular Biology, Bio 21 Molecular Sciences and Biotechnology Institute, University of Melbourne, Parkville, Victoria, Australia
| | - Katrina M Bell
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
| | - James G Fox
- MIT, Department of Comparative Medicine, Boston, Massachusetts, USA
| | - Eva Dimitriadis
- Prince Henrys Institute, Monash University, Clayton, Victoria, Australia
| | - Trevelyan R Menheniott
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
| | - Andrew S Giraud
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia,Department of Paediatrics, University of Melbourne, Royal Children’s Hospital, Flemington Road, Parkville, Victoria, Australia
| | - Louise M Judd
- Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia,Department of Paediatrics, University of Melbourne, Royal Children’s Hospital, Flemington Road, Parkville, Victoria, Australia
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Analysis of Helicobacter pylori cagA promoter elements required for salt-induced upregulation of CagA expression. Infect Immun 2012; 80:3094-106. [PMID: 22710874 DOI: 10.1128/iai.00232-12] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022] Open
Abstract
Helicobacter pylori infection and consumption of a high-salt diet are each associated with an increased risk for the development of gastric cancer. To investigate potential synergism between these factors, we used a global proteomic approach to analyze H. pylori strains cultured in media containing varying salt concentrations. Among the differentially expressed proteins identified, CagA exhibited the greatest increase in expression in response to high salt concentrations. Analysis of 36 H. pylori strains isolated from patients in two regions of Colombia with differing incidences of gastric cancer revealed marked differences among strains in salt-responsive CagA expression. Sequence analysis of the cagA promoter region in these strains revealed a DNA motif (TAATGA) that was present in either one or two copies. Salt-induced upregulation of CagA expression was detected more commonly in strains containing two copies of the TAATGA motif than in strains containing one copy. Mutagenesis experiments confirmed that two copies of the TAATGA motif are required for salt-induced upregulation of CagA expression. In summary, there is considerable heterogeneity among H. pylori strains in salt-regulated CagA expression, and these differences are attributable to variation in a specific DNA motif upstream of the cagA transcriptional start site.
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39
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Minimizing the cancer-promotional activity of cox-2 as a central strategy in cancer prevention. Med Hypotheses 2012; 78:45-57. [DOI: 10.1016/j.mehy.2011.09.039] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/18/2011] [Accepted: 09/19/2011] [Indexed: 02/06/2023]
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Matsuo T, Ito M, Takata S, Tanaka S, Yoshihara M, Chayama K. Low prevalence of Helicobacter pylori-negative gastric cancer among Japanese. Helicobacter 2011; 16:415-9. [PMID: 22059391 DOI: 10.1111/j.1523-5378.2011.00889.x] [Citation(s) in RCA: 170] [Impact Index Per Article: 12.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND AND AIMS The true prevalence of Helicobacter pylori-negative gastric cancer (HpNGC) is unknown. We attempt to clarify the prevalence and clinicopathologic features of HpNGC in Japanese. METHODS Helicobacter pylori infection was detected by antibody titer and microscopic observation. In addition, we confirmed the lack of endoscopic atrophy and histologic gastritis. In these cases, we added urea breath test or rapid urease test to confirm the absence of H. pylori. The mucus phenotype of gastric cancer tissue was also evaluated by immunohistochemistry. RESULTS We screened 3161 gastric cancer cases from 1996 to 2010, and 21 cases were regarded as H. pylori negative. Clinically, patients with HpNGC were younger than patients with H. pylori-positive gastric cancer (controls), and revealed a lack of male dominancy. Histologically, diffuse type was frequently found. All patients examined were pepsinogen negative. Among HpNGC cases with endoscopic resection, the depressed macroscopic appearance was dominant. The prevalence of HpNGC was calculated as 0.66% (95% confidence interval = 0.41-1.01). The mucus phenotype of HpNGC was similar to that of the controls. CONCLUSION The prevalence of HpNGC is very low and its pathological characteristics are different from common gastric cancer.
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Affiliation(s)
- Taiji Matsuo
- Department of Medicine and Molecular Science, Hiroshima University Hiroshima, Japan
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41
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Takamura A, Ito M, Imagawa S, Takata S, Tanaka S, Teixeira CR, Kamada T, Haruma K, Chayama K. Helicobacter pylori cagA polymorphism and gastric inflammation: an international comparison between Japanese and Brazilian patients. Scand J Gastroenterol 2011; 46:1051-1056. [PMID: 21736532 DOI: 10.3109/00365521.2011.598549] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE Gastritis induced by Helicobacter pylori can cause the onset of gastric cancer, and H. pylori cytotoxin associated gene A (cagA) is considered to be an important factor for its development. We investigated the relationship between the grades of gastritis and cagA phenotype in Japanese and Brazilian patients. MATERIAL AND METHODS We studied 47 Brazilian and 47 age-, gender-matched Japanese patients. Status of H. pylori infection, the degree of histologic gastritis, and the levels of serum pepsinogen levels were evaluated. DNA was extracted from paraffin-embedded sections and a portion of the cagA gene was amplified using the polymerase chain reaction, followed by direct sequencing of the fragment. We investigated the cagA subtype using a newly developed restriction fragment length polymorphism (RFLP) system. RESULTS In H. pylori-positive patients, the grades of histological and serological gastritis were more prominent in the Japanese subjects than their Brazilian counterparts, although no difference was detected in the H. pylori-negative subjects. According to cagA phenotype analysis, our RFLP system was helpful for evaluating cagA phenotype, and we found that the prevalence of the East Asia subtype was significantly higher in the Japanese subjects than in the Brazilian. CONCLUSION Infection with H. pylori possessing the East Asian cagA gene contributes to the progression of gastritis.
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Affiliation(s)
- Akemi Takamura
- Department of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan
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Park B, Shin A, Park SK, Ko KP, Ma SH, Lee EH, Gwack J, Jung EJ, Cho LY, Yang JJ, Yoo KY. Ecological study for refrigerator use, salt, vegetable, and fruit intakes, and gastric cancer. Cancer Causes Control 2011; 22:1497-502. [PMID: 21805052 DOI: 10.1007/s10552-011-9823-7] [Citation(s) in RCA: 46] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/29/2011] [Accepted: 07/16/2011] [Indexed: 12/13/2022]
Abstract
We used an ecological approach to determine the correlation between vegetable, fruit and salt intakes, refrigerator use, and gastric cancer mortality in Korean population. Information on fruit and vegetable intakes per capita from the National Health and Nutrition Survey, death certificate data from the National Statistical office, refrigerator per household data from Korean Statistical Information Service, and salt/sodium intake data from a cross-sectional survey were utilized. Correlation coefficients were calculated between vegetable and fruit intakes, refrigerator per household, and gastric cancer mortality and between salt and sodium intakes, and gastric cancer mortality and incidence in the four areas. With 5, 10, and 15 years lag time, refrigerator usage and fruit intake were negatively associated with gastric cancer mortality (p < 0.01), but vegetable intake was not associated with gastric cancer mortality. When estimates of salt/sodium intake evaluated by 24-h urine collection in four areas of Korea were compared to the gastric cancer mortality and incidence in these regions, positive correlation was shown between salt/sodium intake, and gastric cancer incidence and mortality. Negative associations between refrigerator use, fruit intake, and gastric cancer mortality and positive associations between salt/sodium intake and gastric cancer mortality and incidence were suggested.
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Affiliation(s)
- Boyoung Park
- Department of Preventive Medicine, Seoul National University College of Medicine, 103 Daehangno, Chongno-gu, Seoul, Korea
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Peleteiro B, Lopes C, Figueiredo C, Lunet N. Salt intake and gastric cancer risk according to Helicobacter pylori infection, smoking, tumour site and histological type. Br J Cancer 2011; 104:198-207. [PMID: 21081930 PMCID: PMC3039805 DOI: 10.1038/sj.bjc.6605993] [Citation(s) in RCA: 84] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/04/2010] [Revised: 10/08/2010] [Accepted: 10/19/2010] [Indexed: 02/07/2023] Open
Abstract
BACKGROUND Although salt intake is considered a probable risk factor for gastric cancer, relevant studies have provided heterogeneous results, and the magnitude of the association has not been accurately quantified. METHODS To quantify gastric cancer risk in relation to dietary salt exposure according to Helicobacter pylori infection status and virulence, smoking, tumour site, and histological type, we evaluated 422 gastric cancer cases and 649 community controls. Salt exposure was estimated in the year before the onset of symptoms through: sodium intake (estimated by a food frequency questionnaire (FFQ)); main food items/groups contributing to dietary sodium intake; visual analogical scale for salt intake preference; use of table salt; and duration of refrigerator ownership. RESULTS Comparing subjects with the highest with those with the lowest salt exposure (3rd vs 1st third), sodium intake (OR=2.01, 95% CI: 1.16-3.46), consumption of food items with high contribution to sodium intake (OR=2.54, 95% CI: 1.56-4.14) and salt intake evaluated by visual analogical scale (OR=1.83, 95% CI: 1.28-2.63) were associated with an increased gastric cancer risk. Subjects owning a refrigerator for >50 years had a lower risk for gastric cancer (OR=0.28, 95% CI: 0.14-0.57). These associations were observed regardless of H. pylori infection status and virulence, smoking, tumour site or histological type. CONCLUSION Our results support the view that salt intake is an important dietary risk factor for gastric cancer, and confirms the evidence of no differences in risk according to H. pylori infection and virulence, smoking, tumour site and histological type.
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Affiliation(s)
- B Peleteiro
- Department of Hygiene and Epidemiology, Faculty of Medicine, University of Porto, Porto, Portugal.
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Helicobacter pylori and gastric cancer: factors that modulate disease risk. Clin Microbiol Rev 2010; 23:713-39. [PMID: 20930071 DOI: 10.1128/cmr.00011-10] [Citation(s) in RCA: 993] [Impact Index Per Article: 66.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium. In this review, we discuss the host immune response and examine other host factors that increase the pathogenic potential of this bacterium, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors. In addition to host effects and responses, H. pylori strains are genetically diverse. We discuss the main virulence determinants in H. pylori strains and the correlation between these and the diverse clinical outcomes following H. pylori infection. Since H. pylori inhibits the gastric epithelium of half of the world, it is crucial that we continue to gain understanding of host and microbial factors that increase the risk of developing more severe clinical outcomes.
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45
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Inhibitory effects of Japanese apricot (Prunus mume Siebold et Zucc.; Ume) on Helicobacter pylori-related chronic gastritis. Eur J Clin Nutr 2010; 64:714-9. [DOI: 10.1038/ejcn.2010.70] [Citation(s) in RCA: 47] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
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46
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47
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Wang XQ, Terry PD, Yan H. Review of salt consumption and stomach cancer risk: epidemiological and biological evidence. World J Gastroenterol 2009; 15:2204-13. [PMID: 19437559 PMCID: PMC2682234 DOI: 10.3748/wjg.15.2204] [Citation(s) in RCA: 121] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/05/2009] [Revised: 03/23/2009] [Accepted: 03/30/2009] [Indexed: 02/06/2023] Open
Abstract
Stomach cancer is still the fourth most common cancer; thus, it remains an important public health burden worldwide, especially in developing countries. The remarkable geographic variations in the rates of stomach cancer indicate that dietary factors, including a range of food groups to which salt and/or nitrates have been added, may affect stomach cancer risk. In this paper, we review the results from ecologic, case-control and cohort studies on the relationship between salt or salted foods and stomach cancer risk. The majority of ecological studies indicated that the average salt intake in each population was closely correlated with gastric cancer mortality. Most case-control studies showed similar results, indicating a moderate to high increase in risk for the highest level of salt or salted food consumption. The overall results from cohort studies are not totally consistent, but are suggestive of a moderate direct association. Since salt intake has been correlated with Helicobacter pylori (H pylori) infection, it is possible that these two factors may synergize to promote the development of stomach cancer. Additionally, salt may also cause stomach cancer through directly damaging gastric mucus, improving temporary epithelial proliferation and the incidence of endogenous mutations, and inducing hypergastrinemia that leads to eventual parietal cell loss and progression to gastric cancer. Based on the considerable evidence from ecological, case-control and cohort studies worldwide and the mechanistic plausibility, limitation on salt and salted food consumption is a practical strategy for preventing gastric cancer.
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Yanaoka K, Oka M, Yoshimura N, Mukoubayashi C, Enomoto S, Iguchi M, Magari H, Utsunomiya H, Tamai H, Arii K, Yamamichi N, Fujishiro M, Takeshita T, Mohara O, Ichinose M. Risk of gastric cancer in asymptomatic, middle-aged Japanese subjects based on serum pepsinogen andHelicobacter pyloriantibody levels. Int J Cancer 2008; 123:917-26. [DOI: 10.1002/ijc.23571] [Citation(s) in RCA: 57] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]
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Abstract
Epidemiological evidence links high-salt diets and Helicobacter pylori infection with increased risk of developing gastric maladies. The mechanism by which elevated sodium chloride content causes these manifestations is unclear. Here we characterize the response of H. pylori to temporal changes in sodium chloride concentration and show that growth, cell morphology, survival, and virulence factor expression are all altered by increased salt concentration.
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Ghadimi R, Taheri H, Suzuki S, Kashifard M, Hosono A, Esfandiary I, Moghadamnia AA, Ghadimi R, Tokudome S. Host and environmental factors for gastric cancer in Babol, the Caspian Sea Coast, Iran. Eur J Cancer Prev 2007; 16:192-5. [PMID: 17415089 DOI: 10.1097/01.cej.0000220639.61717.67] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
To clarify host and environmental factors for gastric carcinogenesis, we obtained information about gastric cancer mortality in Babol, in the North of Iran, and recruited 130 participants aged 30-80 years from the general population of Babol in 2004. A urea breath test, assessment of IgG antibodies to Helicobacter pylori, a pepsinogen test, a marker of chronic atrophic gastritis, and determination of urinary excretions of sodium and potassium were performed. Diet and lifestyle information was also obtained using a questionnaire. The stomach cancer mortality rate for men in Babol (38.2/10(5)) was found to be somewhat lower than that for Japanese men (45.1/10(5)), while the mortality for women (26.9/10(5)) was higher than for Japanese women (20.9/10(5)). Positive rates for the urea breath test were 77.5 and 81.8% for Iranian men and women, respectively. Helicobacter pylori IgG antibodies were present in 68.7 and 73.7% of Iranian men and women, respectively, both values being marginally higher than for Japanese. We also found 51.0 and 52.8% to be positive for a pepsinogen test, significantly higher than the Japanese values. Urinary excretions of salt and potassium in this population appeared approximately the same as the consumption in Japanese. The elevated gastric cancer mortality in both men and women in Babol seems, by and large, to be related to higher H. pylori infection rates and prevalence of chronic atrophic gastritis. Certain factors, including H. pylori DNA diversity, host factors and their interactions, together with the level of medical practice, prevalence of and access to secondary prevention of stomach cancer, may also be associated with the relatively high mortality.
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Affiliation(s)
- Reza Ghadimi
- Department of Health Promotion and Preventive Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
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