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Morris MT, Piazuelo MB, Olfert IM, Xu X, Hussain S, Peek RM, Busada JT. Chronic cigarette smoke exposure masks pathological features of Helicobacter pylori infection while promoting tumor initiation. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2024:2024.08.05.604297. [PMID: 39211175 PMCID: PMC11361028 DOI: 10.1101/2024.08.05.604297] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/04/2024]
Abstract
Gastric cancer is the fifth most common cancer and the fifth leading cause of cancer deaths worldwide. Chronic infection by the bacterium Helicobacter pylori is the most prominent gastric cancer risk factor, but only 1-3% of infected individuals will develop gastric cancer. Cigarette smoking is another independent gastric cancer risk factor, and H. pylori- infected smokers are at a 2-11-fold increased risk of gastric cancer development, but the direct impacts of cigarette smoke on H. pylori pathogenesis remain unknown. In this study, male C57BL/6 mice were infected with H. pylori and began smoking within one week of infection. The mice were exposed to cigarette smoke (CS) five days/week for 8 weeks. CS exposure had no notable impact on gross gastric morphology or inflammatory status compared to filtered-air (FA) exposed controls in mock-infected mice. However, CS exposure significantly blunted H. pylori- induced gastric inflammatory responses, reducing gastric atrophy and pyloric metaplasia development. Despite blunting these classic pathological features of H. pylori infection, CS exposures increased DNA damage within the gastric epithelial cells and accelerated H. pylori- induced dysplasia onset in the INS-GAS gastric cancer model. These data suggest that cigarette smoking may clinically silence classic clinical symptoms of H. pylori infection but enhance the accumulation of mutations and accelerate gastric cancer initiation.
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Hatta W, Koike T, Asano N, Hatayama Y, Ogata Y, Saito M, Jin X, Uno K, Imatani A, Masamune A. The Impact of Tobacco Smoking and Alcohol Consumption on the Development of Gastric Cancers. Int J Mol Sci 2024; 25:7854. [PMID: 39063094 PMCID: PMC11276971 DOI: 10.3390/ijms25147854] [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] [Received: 06/21/2024] [Revised: 07/09/2024] [Accepted: 07/12/2024] [Indexed: 07/23/2024] Open
Abstract
Chronic infection of Helicobacter pylori is considered the principal cause of gastric cancers, but evidence has accumulated regarding the impact of tobacco smoking and alcohol consumption on the development of gastric cancers. Several possible mechanisms, including the activation of nicotinic acetylcholine receptors, have been proposed for smoking-induced gastric carcinogenesis. On the other hand, local acetaldehyde exposure and ethanol-induced mucosal inflammation have been proposed as the mechanisms involved in the development of gastric cancers in heavy alcohol drinkers. In addition, genetic polymorphisms are also considered to play a pivotal role in smoking-related and alcohol-related gastric carcinogenesis. In this review, we will discuss the molecular mechanisms involved in the development of gastric cancers in relation to tobacco smoking and alcohol consumption.
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Affiliation(s)
- Waku Hatta
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Tomoyuki Koike
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Naoki Asano
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
- Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, 47-1 Nodayama, Medeshima-Shiode, Natori 981-1293, Miyagi, Japan
- Division of Carcinogenesis and Senescence Biology, Tohoku University Graduate School of Medicine, Natori 981-1293, Miyagi, Japan
| | - Yutaka Hatayama
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Yohei Ogata
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Masahiro Saito
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Xiaoyi Jin
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Kaname Uno
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Akira Imatani
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Atsushi Masamune
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
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Abellán Alemán J, Sabaris RC, Pardo DE, García Donaire JA, Romanos FG, Iriso JI, Penagos LM, Iglesias LJN, de Salinas APM, Pérez-Monteoliva NRR, Lezcano PSR, Saborido MT, Roca FV. Documento de consenso sobre tabaquismo y riesgo vascular. HIPERTENSION Y RIESGO VASCULAR 2024; 41 Suppl 1:S1-S85. [PMID: 38729667 DOI: 10.1016/s1889-1837(24)00075-8] [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] [Indexed: 05/12/2024]
Abstract
Consensus statement on smoking and vascular risk About 22% of the Spanish population are daily smokers. Men are more likely to smoke than women. In Spain, women between 15-25 years of age smoke as much or more than men. Every smoker should be assessed for: physical dependence on nicotine (Fagerström test), social and psychological dependence (Glover Nilsson test), level of motivation to quit (Richmond test), probability of therapy success (Henri-Mondor and Michael-Fiore tests), and stage of behavioral change development (Prochaska and DiClementi). Advice on smoking cessation is highly cost-effective and should always be provided. Smoking is an enhancer of cardiovascular risk because it acts as a pathogen agent in the development of arteriosclerosis and is associated with ischemic heart disease, stroke, and peripheral artery disease. Smoking increases the risk of chronic lung diseases (COPD) and is related to cancers of the lung, female genitalia, larynx, oropharynx, bladder, mouth, esophagus, liver and biliary tract, and stomach, among others. Combined oral contraceptives should be avoided in women smokers older than 35 years of age due to the risk of thromboembolism. In smoking cessation, the involvement of physicians, nurses, psychologists, etc. is important, and their multidisciplinary collaboration is needed. Effective pharmacological treatments for smoking cessation are available. Combined treatments are recommended when smoker's dependence is high. For individuals who are unable to quit smoking, a strategy based on tobacco damage management with a total switch to smokeless products could be a less dangerous alternative for their health than continuing to smoke.
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Affiliation(s)
- José Abellán Alemán
- Sociedad Murciana de Hipertensión Arterial y Riesgo Cardiovascular, Cátedra de Riesgo Cardiovascular, Universidad Católica de Murcia, Murcia, España.
| | - Rafael Crespo Sabaris
- Sociedad Riojana de Hipertensión y Riesgo Vascular, Centro de Salud de Entrena, La Rioja, España
| | - Daniel Escribano Pardo
- Sociedad Aragonesa de Hipertensión y Riesgo Vascular, Centro de Salud Oliver, Zaragoza, España
| | - José Antonio García Donaire
- Sociedad Española de Hipertensión, Unidad de Hipertensión, Servicio de Medicina Interna, Hospital Clínico Universitario San Carlos, Madrid, España
| | - Fernando García Romanos
- Sociedad de Hipertensión y Riesgo Vascular de las Illes Balears, Centro de Salud Santa Catalina, Palma de Mallorca, España
| | - Jesús Iturralde Iriso
- Sociedad Vasca de Hipertensión y Riesgo Vascular, Centro de Salud la Habana-Cuba, Vitoria-Gasteiz, España
| | - Luis Martín Penagos
- Sociedad Cántabra de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital Universitario Marqués de Valdecilla, Santander, España
| | - L Javier Nieto Iglesias
- Sociedad Castilla-La Mancha de Hipertensión y Riesgo Vascular, Unidad de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital General Universitario de Ciudad Real, Ciudad Real, España
| | - Alfonso Pobes Martínez de Salinas
- Sociedad Asturiana de Hipertensión y Riesgo Vascular, Área de Gestión Clínica, Interáreas de Nefrología VII y VIII del SESPA, Asturias, España
| | | | - Pablo Sánchez-Rubio Lezcano
- Sociedad Aragonesa de Hipertensión y Riesgo Vascular, Servicio de Medicina Interna, Hospital General Universitario San Jorge, Huesca, España
| | - Maribel Troya Saborido
- Sociedad Catalana de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, España
| | - Francisco Valls Roca
- Sociedad Valenciana de Hipertensión y Riesgo Vascular, Centro de Salud de Beniganim, Valencia, España
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Rota M, Possenti I, Valsassina V, Santucci C, Bagnardi V, Corrao G, Bosetti C, Specchia C, Gallus S, Lugo A. Dose-response association between cigarette smoking and gastric cancer risk: a systematic review and meta-analysis. Gastric Cancer 2024; 27:197-209. [PMID: 38231449 DOI: 10.1007/s10120-023-01459-1] [Citation(s) in RCA: 12] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/28/2023] [Accepted: 12/16/2023] [Indexed: 01/18/2024]
Abstract
This study aims at providing an accurate and up-to-date quantification of the dose-response association between cigarette smoking and gastric cancer (GC) risk, overall and by subsite. We conducted a systematic review and meta-analysis of case-control and cohort studies on the association between cigarette smoking and GC risk published up to January 2023. We estimated pooled relative risks (RR) of GC and its subsites according to smoking status, intensity, duration, and time since quitting. Among 271 eligible articles, 205 original studies were included in this meta-analysis. Compared with never smokers, the pooled RR for GC was 1.53 (95% confidence interval; CI 1.44-1.62; n = 92) for current and 1.30 (95% CI 1.23-1.37; n = 82) for former smokers. The RR for current compared with never smokers was 2.08 (95% CI 1.66-2.61; n = 21) for gastric cardia and 1.48 (95% CI 1.33-1.66; n = 8) for distal stomach cancer. GC risk nonlinearly increased with smoking intensity up to 20 cigarettes/day (RR:1.69; 95% CI 1.55-1.84) and levelled thereafter. GC risk significantly increased linearly with increasing smoking duration (RR: 1.31; 95% CI 1.25-1.37 for 20 years) and significantly decreased linearly with increasing time since quitting (RR: 0.65; 95% CI 0.44-0.95 for 30 years since cessation). The present meta-analysis confirms that cigarette smoking is an independent risk factor for GC, particularly for gastric cardia. GC risk increases with a low number of cigarettes up to 20 cigarettes/day and increases in a dose-dependent manner with smoking duration.
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Affiliation(s)
- Matteo Rota
- Department of Molecular and Translational Medicine, Università Degli Studi Di Brescia, Brescia, Italy
| | - Irene Possenti
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy
| | - Valeria Valsassina
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy
| | - Claudia Santucci
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
| | - Vincenzo Bagnardi
- Department of Statistics and Quantitative Methods, Università Degli Studi Di Milano-Bicocca, Milan, Italy
| | - Giovanni Corrao
- Laboratory of Healthcare Research and Pharmacoepidemiology, Unit of Biostatistics, Epidemiology and Public Health, Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy
- National Centre of Healthcare Research and Pharmacoepidemiology, University of Milano-Bicocca, Milan, Italy
| | - Cristina Bosetti
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy
| | - Claudia Specchia
- Department of Molecular and Translational Medicine, Università Degli Studi Di Brescia, Brescia, Italy
| | - Silvano Gallus
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy
| | - Alessandra Lugo
- Department of Medical Epidemiology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.
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Tan Y, Wei Z, Liu K, Qin Y, Hui W. Lifestyle habits and gastric cancer in an East Asian population: a Mendelian randomization study. Front Oncol 2023; 13:1224753. [PMID: 37731647 PMCID: PMC10507616 DOI: 10.3389/fonc.2023.1224753] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/25/2023] [Accepted: 08/14/2023] [Indexed: 09/22/2023] Open
Abstract
Background Epidemiological evidence suggests an association between lifestyle habits (smoking, alcohol consumption, tea, coffee intake, etc.) and gastric cancer (GC). However, the causal relationship remains uncertain. Therefore, the purpose of this study was to ascertain whether there is a causal connection between them. Methods Two-sample Mendelian randomization (MR) analysis was performed using the publicly available Genome Wide Association Study summary datasets using six methods: inverse variance weighting (IVW), weighted median, MR using a Robust Adjusted Profile Score (MR.Raps), MR using a Robust Adjusted Profile Score (MR-PRESSO), Radial regression of MR, and Causal Analysis Using Summary Effect Estimates (CAUSE). A sensitivity analysis was conducted to assess the robustness of the results. Results In an East Asian population, we found that increased tea intake reduced the risk of GC [odds ratio (OR)= 0.90, 95% confidence interval (CI)= 0.82-0.99, P = 0.037] while there was a positive association between smoking and GC (OR = 1.58, 95% CI = 1.04-2.39, P = 0.032). No causal relationship between alcohol and coffee intake and GC. Sensitivity analyses demonstrated the robustness of these causal associations. Conclusions Our study suggests that tea intake may reduce the risk of GC, for which smoking is a potential risk factor. Nevertheless, a larger and more diverse sample size is needed for further validation.
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Affiliation(s)
- Yuegui Tan
- Department of Pharmacy, Xi’an Fifth Hospital, Xian, Shaanxi, China
| | - Zhao Wei
- Department of Medicinal Chemistry, School of Pharmacy, Air Force Medical University, Xi’an, Shaanxi, China
| | - Kun Liu
- Department of Epidemiology, Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Air Force Medical University, Xi’an, Shaanxi, China
| | - Yuzhen Qin
- Xi’an Jiaotong-liverpool University, XJTLU Wisdom Lake Academy of Pharmacy, Xian, Shaanxi, China
| | - Wenqi Hui
- Department of Pharmacy, Xi’an Fifth Hospital, Xian, Shaanxi, China
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Patrad E, Khalighfard S, Amiriani T, Khori V, Alizadeh AM. Molecular mechanisms underlying the action of carcinogens in gastric cancer with a glimpse into targeted therapy. Cell Oncol 2022; 45:1073-1117. [PMID: 36149600 DOI: 10.1007/s13402-022-00715-3] [Citation(s) in RCA: 13] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 09/03/2022] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Gastric cancer imposes a substantial global health burden despite its overall incidence decrease. A broad spectrum of inherited, environmental and infectious factors contributes to the development of gastric cancer. A profound understanding of the molecular underpinnings of gastric cancer has lagged compared to several other tumors with similar incidence and morbidity rates, owing to our limited knowledge of the role of carcinogens in this malignancy. The International Agency for Research on Cancer (IARC) has classified gastric carcinogenic agents into four groups based on scientific evidence from human and experimental animal studies. This review aims to explore the potential comprehensive molecular and biological impacts of carcinogens on gastric cancer development and their interactions and interferences with various cellular signaling pathways. CONCLUSIONS In this review, we highlight recent clinical trial data reported in the literature dealing with different ways to target various carcinogens in gastric cancer. Moreover, we touch upon other multidisciplinary therapeutic approaches such as surgery, adjuvant and neoadjuvant chemotherapy. Rational clinical trials focusing on identifying suitable patient populations are imperative to the success of single-agent therapeutics. Novel insights regarding signaling pathways that regulate gastric cancer can potentially improve treatment responses to targeted therapy alone or in combination with other/conventional treatments. Preventive strategies such as control of H. pylori infection through eradication or immunization as well as dietary habit and lifestyle changes may reduce the incidence of this multifactorial disease, especially in high prevalence areas. Further in-depth understanding of the molecular mechanisms involved in the role of carcinogenic agents in gastric cancer development may offer valuable information and update state-of-the-art resources for physicians and researchers to explore novel ways to combat this disease, from bench to bedside. A schematic outlining of the interaction between gastric carcinogenic agents and intracellular pathways in gastric cancer H. pylori stimulates multiple intracellular pathways, including PI3K/AKT, NF-κB, Wnt, Shh, Ras/Raf, c-MET, and JAK/STAT, leading to epithelial cell proliferation and differentiation, apoptosis, survival, motility, and inflammatory cytokine release. EBV can stimulate intracellular pathways such as the PI3K/Akt, RAS/RAF, JAK/STAT, Notch, TGF-β, and NF-κB, leading to cell survival and motility, proliferation, invasion, metastasis, and the transcription of anti-apoptotic genes and pro-inflammatory cytokines. Nicotine and alcohol can lead to angiogenesis, metastasis, survival, proliferation, pro-inflammatory, migration, and chemotactic by stimulating various intracellular signaling pathways such as PI3K/AKT, NF-κB, Ras/Raf, ROS, and JAK/STAT. Processed meat contains numerous carcinogenic compounds that affect multiple intracellular pathways such as sGC/cGMP, p38 MAPK, ERK, and PI3K/AKT, leading to anti-apoptosis, angiogenesis, metastasis, inflammatory responses, proliferation, and invasion. Lead compounds may interact with multiple signaling pathways such as PI3K/AKT, NF-κB, Ras/Raf, DNA methylation-dependent, and epigenetic-dependent, leading to tumorigenesis, carcinogenesis, malignancy, angiogenesis, DNA hypermethylation, cell survival, and cell proliferation. Stimulating signaling pathways such as PI3K/Akt, RAS/RAF, JAK/STAT, WNT, TGF-β, EGF, FGFR2, and E-cadherin through UV ionizing radiation leads to cell survival, proliferation, and immortalization in gastric cancer. The consequence of PI3K/AKT, NF-κB, Ras/Raf, ROS, JAK/STAT, and WNT signaling stimulation by the carcinogenic component of Pickled vegetables and salted fish is the Warburg effect, tumorigenesis, angiogenesis, proliferation, inflammatory response, and migration.
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Affiliation(s)
- Elham Patrad
- Cancer Research Center, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Solmaz Khalighfard
- Cancer Research Center, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Taghi Amiriani
- Ischemic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran
| | - Vahid Khori
- Ischemic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran
| | - Ali Mohammad Alizadeh
- Cancer Research Center, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran.
- Breast Disease Research Center, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran.
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Associations of Duration, Intensity, and Quantity of Smoking With Risk of Gastric Intestinal Metaplasia. J Clin Gastroenterol 2022; 56:e71-e76. [PMID: 33337636 PMCID: PMC8875544 DOI: 10.1097/mcg.0000000000001479] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/14/2020] [Accepted: 11/09/2020] [Indexed: 12/12/2022]
Abstract
GOAL Determine whether various dimensions of smoking increase risk for gastric intestinal metaplasia. BACKGROUND Cigarette smoking has been implicated in the etiology of gastric cancer, but it is not clear if smoking is a risk factor for gastric intestinal metaplasia, a precursor lesion of gastric cancer. MATERIALS AND METHODS We compared data from 385 gastric intestinal metaplasia cases and 1577 controls without gastric intestinal metaplasia recruited into a cross-sectional study at the Michael E. DeBakey VA Medical Center in Houston, Texas. All participants completed standardized questionnaires and underwent a study endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included participants with intestinal metaplasia on any noncardia gastric biopsy. We calculated odds ratios and associated 95% confidence intervals using multivariable logistic regression models. RESULTS Compared with never smokers, current smokers had 2-fold increased risk for gastric intestinal metaplasia (odds ratio, 2.05; 95% confidence interval, 1.47-2.85). Among ever smokers, increasing duration and total dose were significantly associated with increased risk for gastric intestinal metaplasia (P-trend, 0.004 and 0.01, respectively). Among former smokers, risk for gastric intestinal metaplasia decreased over time and was no different to never smokers after 15 years smoking cessation. Cases with gastric intestinal metaplasia were more likely than controls to have Helicobacter pylori infection (53.2% vs. 21.7%); however, smoking effect on gastric intestinal metaplasia was not different by H. pylori infection status. CONCLUSIONS Cigarette smoking is a risk factor for gastric intestinal metaplasia. Risk of gastric intestinal metaplasia among former smokers remained significantly elevated until 15 years postcessation.
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Nguyen NLT, Dang NDT, Dang QH, Tran VC, Vo HL, Yamaguchi M, Ta TV. Polymorphism of MUC1 Gene in Vietnamese Gastric Cancer Patients: A Multicenter Case-Control Study. Front Oncol 2021; 11:694977. [PMID: 34532288 PMCID: PMC8439541 DOI: 10.3389/fonc.2021.694977] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/14/2021] [Accepted: 08/10/2021] [Indexed: 12/31/2022] Open
Abstract
Background A few studies revealed that the polymorphisms of Mucin 1 gene have a role and significance as a susceptible factor contributing to gastric cancer. To better understand the roles of two MUC1 genotype polymorphisms of rs4072037 and rs2070803 in the development of gastric cancer in Vietnamese population, a multicenter, large-sample, case-control study was conducted to investigate the potential association of these single-nucleotide polymorphisms (SNPs) of MUC1 gene with gastric cancer risk and to evaluate the combination factors in relation with these SNPs. Methods This case-control study included 302 gastric cancer patients and 304 controls at four national medical hospitals between 2016 and 2018. All participants were interviewed for sociodemographic characteristics, smoking and drinking status, and personal and family history of gastric diseases. Genotyping was done using polymerase chain reaction-restriction fragment length polymorphism analysis. The association of SNPs with gastric cancer was explored using logistic regression models. Results AA genotype for rs4072037 was significantly associated with increased gastric cancer. Those with AA genotype had higher gastric cancer risk than had patients with AG (OR: 2.09, 95% CI: 1.48-2.96) and a combination of AG+GG (OR: 1.85, 95% CI: 1.33-2.56). In rs2070803, GG genotype increased gastric cancer risk when compared with AG (OR: 1.97, 95% CI: 1.39-2.80) and AG+AA (OR: 1.71, 95% CI: 1.23-2.39). AG genotypes in both SNPs decreased gastric cancer risk when compared with homogenous genotype, more specifically AA (OR: 0.51, 95% CI: 0.35-0.72) and GG (OR: 0.58, 95% CI: 0.35-0.97). These genotypes in combination with above-60-year-old age, male gender, alcoholism, and personal history of gastric disease were also significantly elevated risk factors for gastric cancer. Conclusions rs4072037 and rs2070803 of Mucin 1 genes are two genotypic risk factors for gastric cancer. Those in combination with gender, family history, smoking, and drinking habits significantly increase the risk of gastric cancer.
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Affiliation(s)
- Ngoc-Lan Thi Nguyen
- Biochemistry Department, Hanoi Medical University, Hanoi, Vietnam.,Clinical Laboratory, Hanoi Medical University Hospital, Hanoi Medical University, Hanoi, Vietnam
| | - Ngoc-Dzung Thi Dang
- Biochemistry Department, Hanoi Medical University, Hanoi, Vietnam.,Clinical Laboratory, Hanoi Medical University Hospital, Hanoi Medical University, Hanoi, Vietnam
| | - Quang-Huy Dang
- Department of Medical Laboratory Science, Faculty of Medical Technology, Hanoi Medical University, Hanoi, Vietnam
| | - Van-Chuc Tran
- Biochemistry Department, Hanoi Medical University, Hanoi, Vietnam
| | - Hoang-Long Vo
- Department of Scientific Research and International Cooperation, Hanoi Medical University Hospital, Hanoi Medical University, Hanoi, Vietnam
| | - Masamitsu Yamaguchi
- Department of Applied Biology, Advanced Insect Research Promotion Center, Kyoto Institute of Technology, Kyoto, Japan
| | - Thanh-Van Ta
- Biochemistry Department, Hanoi Medical University, Hanoi, Vietnam.,Clinical Laboratory, Hanoi Medical University Hospital, Hanoi Medical University, Hanoi, Vietnam
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Poorolajal J, Heidarimoghis F, Karami M, Cheraghi Z, Gohari-Ensaf F, Shahbazi F, Zareie B, Ameri P, Sahraee F. Factors for the Primary Prevention of Breast Cancer: A Meta-Analysis of Prospective Cohort Studies. J Res Health Sci 2021; 21:e00520. [PMID: 34698654 PMCID: PMC8957681 DOI: 10.34172/jrhs.2021.57] [Citation(s) in RCA: 19] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/01/2021] [Accepted: 07/14/2021] [Indexed: 12/13/2022] Open
Abstract
Background: This report provided the effect of 15 preventable factors on the risk of breast cancer incidence.
Study design: A systematic review and meta-analysis.
Methods: A detailed research was conducted on PubMed, Web of Science, and Scopus databases in January 2020. Reference lists were also screened. Prospective cohort studies addressing the associations between breast cancer and 15 factors were analyzed. Between-study heterogeneity was investigated using the χ2, τ2, and I2 statistics. The probability of publication bias was explored using the Begg and Egger tests and trim-and-fill analysis. Effect sizes were expressed as risk ratios (RRs) with 95% confidence intervals (CIs) using a random-effects model.
Results: Based on the results, out of 147,083 identified studies, 197 were eligible, including 19,413,702 participants. The RRs (95% CI) of factors associated with breast cancer were as follows: cigarette smoking 1.07 (1.05, 1.09); alcohol drinking 1.10 (1.07, 1.12); sufficient physical activity 0.90 (0.86, 0.95); overweight/obesity in premenopausal 0.92 (0.82, 1.03) and postmenopausal 1.18 (1.13, 1.24); nulliparity 1.16 (1.03, 1.31); late pregnancy 1.37 (1.25, 1.50); breastfeeding 0.87 (0.81, 0.93); ever using oral contraceptive 1.00 (0.96, 1.05); ever using estrogen 1.13 (1.04, 1.23); ever using progesterone 1.02 (0.84, 1.24); ever using estrogen/progesterone 1.60 (1.42, 1.80); ever taking hormone replacement therapy 1.26 (1.20, 1.32); red meat consumption 1.05 (1.00, 1.11); fruit/vegetable consumption 0.87 (0.83, 0.90); and history of radiation therapy, based on single study 1.31 (0.87, 1.98).
Conclusions: This meta-analysis provided a clear picture of several factors associated with the development of breast cancer. Moreover, the useful information in this study may be utilized for ranking and prioritizing preventable risk factors to implement effective prevention programs.
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Affiliation(s)
- Jalal Poorolajal
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran. .,Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.,Research Center for Health Sciences, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Fatemeh Heidarimoghis
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Manoochehr Karami
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran.,Social Determinants of Health Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Zahra Cheraghi
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran.,Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Fatemeh Gohari-Ensaf
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Fatemeh Shahbazi
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Bushra Zareie
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Pegah Ameri
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Fatemeh Sahraee
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
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10
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Ohnishi I, Iwashita Y, Matsushita Y, Ohtsuka S, Yamashita T, Inaba K, Fukazawa A, Ochiai H, Matsumoto K, Kurono N, Matsushima Y, Mori H, Suzuki S, Suzuki S, Tanioka F, Sugimura H. Mass spectrometric profiling of DNA adducts in the human stomach associated with damage from environmental factors. Genes Environ 2021; 43:12. [PMID: 33836837 PMCID: PMC8034090 DOI: 10.1186/s41021-021-00186-2] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2021] [Accepted: 03/27/2021] [Indexed: 02/07/2023] Open
Abstract
BACKGROUND A comprehensive understanding of DNA adducts, one of the most plausible origins of cancer mutations, is still elusive, especially in human tissues in clinical settings. Recent technological developments have facilitated the identification of multiple DNA adducts in a single experiment. Only a few attempts toward this "DNA adductome approach" in human tissues have been reported. Geospatial information on DNA adducts in human organs has been scarce. AIM Mass spectrometry of human gastric mucosal DNA was performed to identify DNA adducts associated with environmental factors. MATERIALS AND METHODS From 59 subjects who had received gastrectomy for gastric cancer, 306 samples of nontumor tissues and 15 samples of tumors (14 cases) were taken for DNA adductome analysis. Gastric nontumor tissue from autopsies of 7 subjects without gastric cancer (urothelial cancer, hepatocellular carcinoma, lung cancer each; the other four cases were without any cancers) was also investigated. Briefly, DNA was extracted from each sample with antioxidants, digested into nucleosides, separated by liquid chromatography, and then electrospray-ionized. Specific DNA adducts were identified by mass/charge number and column retention time compared to standards. Information on lifestyle factors such as tobacco smoking and alcohol drinking was taken from the clinical records of each subject. RESULTS Seven DNA adducts, including modified bases, C5-methyl-2'-deoxycytidine, 2'-deoxyinosine, C5-hydroxymethyl-2'-deoxycytidine, N6-methyl-2'-deoxyadenosine, 1,N6-etheno-2'-deoxyadenosine, N6-hydroxymethyl-2'-deoxyadenosine, and C8-oxo-2'-deoxyguanosine, were identified in the human stomach and characterized. Intraindividual differences according to the multiple sites of these adducts were noted but were less substantial than interindividual differences. N6-hydroxymethyl-2'-deoxyadenosine was identified in the human stomach for the first time. The amount of C5-hydroxymethyl-2'-deoxycytidine was higher in the stomachs of subjects without gastric cancer than in the nontumor and tumor portions of the stomach in gastric cancer patients. Higher levels of 1,N6-etheno-2'-deoxyadenosine were detected in the subjects who reported both smoking and drinking than in those without these habits. These DNA adducts showed considerable correlations with each other. CONCLUSIONS We characterized 7 DNA adducts in the nontumor portion of the human stomach in both gastric cancer subjects and nongastric cancer subjects. A reduction in C5-hydroxymethyl-dC even in the nontumor mucosa of patients with gastric cancer was observed. Smoking and drinking habits significantly influenced the quantity of one of the lipid peroxidation-derived adducts, etheno-dA. A more expansive DNA adductome profile would provide a comprehensive understanding of the origin of human cancer in the future.
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Affiliation(s)
- Ippei Ohnishi
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
- Pathology Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Yuji Iwashita
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan.
| | - Yuto Matsushita
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
- Department of Urology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
| | - Shunsuke Ohtsuka
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
- Hamamatsu Medical Center, 328 Tomitsuka-cho, Naka-ku, Hamamatsu, Shizuoka, 432-8580, Japan
| | - Takashi Yamashita
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
- First Department of Surgery, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
| | - Keisuke Inaba
- Surgery Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Atsuko Fukazawa
- Surgery Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Hideto Ochiai
- Surgery Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Keigo Matsumoto
- Surgery Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Nobuhito Kurono
- Department of Chemistry, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan
| | - Yoshitaka Matsushima
- Department of Agricultural Chemistry, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo, 156-8502, Japan
| | - Hiroki Mori
- Hamamatsu Medical Center, 328 Tomitsuka-cho, Naka-ku, Hamamatsu, Shizuoka, 432-8580, Japan
| | - Shioto Suzuki
- Pathology Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Shohachi Suzuki
- Surgery Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Fumihiko Tanioka
- Pathology Division, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan
| | - Haruhiko Sugimura
- Department of Tumor Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan.
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11
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A decade in unravelling the etiology of gastric carcinogenesis in Kashmir, India – A high risk region. GENE REPORTS 2020. [DOI: 10.1016/j.genrep.2020.100832] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
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12
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Li J, Xu HL, Yao BD, Li WX, Fang H, Xu DL, Zhang ZF. Environmental tobacco smoke and cancer risk, a prospective cohort study in a Chinese population. ENVIRONMENTAL RESEARCH 2020; 191:110015. [PMID: 32818497 DOI: 10.1016/j.envres.2020.110015] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 08/25/2019] [Revised: 05/30/2020] [Accepted: 07/27/2020] [Indexed: 06/11/2023]
Abstract
Few prospective cohort studies have investigated associations between environmental tobacco smoke (ETS) and other cancer sites, in addition to lung cancer. We assessed these associations in a population-based prospective cohort study started from 2008 to 2011 with average of 9.1 years of follow-up, in Minhang district, Shanghai, China. The study included a total of 23,415 participants (8388 men, 15,027 women) and 205,515 person-years. Epidemiological data were collected by a standardized questionnaire including ETS exposure. Newly diagnosed patients with primary cancers and deaths were identified by record linkage system with the Shanghai Cancer Registry and Shanghai Vital Statistics. Hazard ratios (HRs) and their 95% confidence intervals (CIs) were estimated using Cox proportional hazards regression models, adjusting for potential confounders. During the study period, a total of 1462 patients with diagnoses of primary cancers were identified. Among all participants and non-smokers, ETS was associated with an increased risk of all smoking-related cancers (all: adjusted HR: 1.23, 95% CI: 1.05-1.43 and non-smokers: 1.24, 1.02-1.49), lung cancer (1.29, 0.98-1.71 and 1.27, 0.91-1.77), and stomach cancer (1.86, 1.21-2.85 and 1.75, 1.05-2.91), respectively. Furthermore, associations for lung and stomach cancers were the strongest among non-smoking females. The joint effects of both ETS and active smoking were strongest for all cancers, all smoking-related cancers, lung cancer, and stomach cancer. No clear interactions were observed. These results suggest that ETS exposure may increase the risk of smoking-related cancers in a Chinese population. Further studies on the relationship between ETS exposure and specific cancer sites are warranted to replicate our findings.
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Affiliation(s)
- Jun Li
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China; Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, CA, 90095, USA
| | - Hui-Lin Xu
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China
| | - Bao-Dong Yao
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China
| | - Wei-Xi Li
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China
| | - Hong Fang
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China
| | - Dong-Li Xu
- Department of Non-Communicable Diseases Prevention and Control, Shanghai Minhang Center for Disease Control and Prevention, Shanghai, 201101, China.
| | - Zuo-Feng Zhang
- Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, CA, 90095, USA.
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13
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Ghosh P, Alam N, Mandal S, Mustafi SM, Murmu N. Association of mTOR pathway with risk of gastric cancer in male smoker with potential prognostic significance. Mol Biol Rep 2020; 47:7489-7495. [PMID: 32918126 DOI: 10.1007/s11033-020-05808-6] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/19/2020] [Accepted: 09/03/2020] [Indexed: 12/13/2022]
Abstract
Aberrant expression of mTOR signaling pathway is significantly associated with gastric cancer. However, the effect of smoking on mTOR expression and its downstream signaling molecules in gastric cancer has not been explored. Our study aims to investigate the effect of smoking on p-mTOR and its correlation with various downstream targets and survival of the smoker and never-smoker in advanced gastric cancer patients. Forty-one smokers and 41 never-smokers patient sample with the advanced gastric carcinoma were chosen for this study. Immunohistochemistry and western blot analysis were performed to check the expression of p-mTOR and its downstream targets. The correlation of p-mTOR with its downstream targets was analyzed by linear regression analysis in Graph Pad Prism software. Survivability analysis was examined by Kaplan-Meier method with log rank test in SPSS. High expression of p-mTOR and its downstream targets were observed in advanced gastric cancer smoker patients as compared to never-smokers by immunohistochemistry and western blot analysis. Results revealed that over expressed p-mTOR in smoker patients were positively correlated with its downstream targets (P < 0.05) and poor survival (P = 0.034). Over expression of p-mTOR in gastric cancer male smoker patients had the worse outcome.
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Affiliation(s)
- Paramita Ghosh
- Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700026, India
| | - Neyaz Alam
- Department of Surgical Oncology, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata, 700026, India
| | - Shyamsundar Mandal
- Department of Epidemiology and Biostatistics, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700026, India
| | - Saunak Mitra Mustafi
- Department of Pathology, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700026, India
| | - Nabendu Murmu
- Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700026, India.
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14
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Poorolajal J, Moradi L, Mohammadi Y, Cheraghi Z, Gohari-Ensaf F. Risk factors for stomach cancer: a systematic review and meta-analysis. Epidemiol Health 2020; 42:e2020004. [PMID: 32023777 PMCID: PMC7056944 DOI: 10.4178/epih.e2020004] [Citation(s) in RCA: 159] [Impact Index Per Article: 31.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/11/2019] [Accepted: 02/02/2020] [Indexed: 02/06/2023] Open
Abstract
OBJECTIVES This report provides information on 14 behavioral and nutritional factors that can be addressed in stomach cancer prevention programs. METHODS PubMed, Web of Science, and Scopus were searched through December 2018. Reference lists were also screened. Observational studies addressing the associations between stomach cancer and behavioral factors were analyzed. Between-study heterogeneity was investigated using the χ2, τ2, and I2 statistics. The likelihood of publication bias was explored using the Begg and Egger tests and trim-and-fill analysis. Effect sizes were expressed as odds ratios (ORs) with 95% confidence intervals (CIs) using a random-effects model. RESULTS Of 52,916 identified studies, 232 (including 33,831,063 participants) were eligible. The OR (95% CI) of factors associated with stomach cancer were as follows: Helicobacter pylori infection, 2.56 (95% CI, 2.18 to 3.00); current smoking, 1.61 (95% CI, 1.49 to 1.75); former smoking 1.43 (95% CI, 1.29 to 1.59); current drinking, 1.19 (95% CI, 1.10 to 1.29); former drinking, 1.73 (95% CI, 1.17 to 2.56); overweight/obesity, 0.89 (95% CI, 0.74 to 1.08); sufficient physical activity, 0.83 (95% CI, 0.68 to 1.02); consumption of fruits ≥3 times/wk, 0.48 (95% CI, 0.37 to 0.63); consumption of vegetables ≥3 times/wk, 0.62 (95% CI, 0.49 to 0.79); eating pickled vegetables, 1.28 (95% CI, 1.09 to 1.51); drinking black tea, 1.00 (95% CI, 0.84 to 1.20); drinking green tea, 0.88 (95% CI, 0.80 to 0.97); drinking coffee, 0.99 (95% CI, 0.88 to 1.11); eating fish ≥1 time/wk 0.79 (95% CI, 0.61 to 1.03); eating red meat ≥4 times/wk 1.31 (95% CI, 0.87 to 1.96), and high salt intake 3.78 (95% CI, 1.74 to 5.44) and 1.34 (95% CI, 0.88 to 2.03), based on two different studies. CONCLUSIONS This meta-analysis provided a clear picture of the behavioral and nutritional factors associated with the development of stomach cancer. These results may be utilized for ranking and prioritizing preventable risk factors to implement effective prevention programs.
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Affiliation(s)
- Jalal Poorolajal
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
- Research Center for Health Sciences, Hamadan University of Medical Sciences, Hamadan, Iran
- Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Leila Moradi
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Younes Mohammadi
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
- Social Determinants of Health Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Zahra Cheraghi
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
- Modeling of Noncommunicable Diseases Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
| | - Fatemeh Gohari-Ensaf
- Department of Epidemiology, School of Public Health, Hamadan University of Medical Sciences, Hamadan, Iran
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15
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Praud D, Rota M, Pelucchi C, Bertuccio P, Rosso T, Galeone C, Zhang ZF, Matsuo K, Ito H, Hu J, Johnson KC, Yu GP, Palli D, Ferraroni M, Muscat J, Lunet N, Peleteiro B, Malekzadeh R, Ye W, Song H, Zaridze D, Maximovitch D, Aragonés N, Castaño-Vinyals G, Vioque J, Navarrete-Muñoz EM, Pakseresht M, Pourfarzi F, Wolk A, Orsini N, Bellavia A, Håkansson N, Mu L, Pastorino R, Kurtz RC, Derakhshan MH, Lagiou A, Lagiou P, Boffetta P, Boccia S, Negri E, La Vecchia C. Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project. Eur J Cancer Prev 2018; 27:124-133. [PMID: 27560662 DOI: 10.1097/cej.0000000000000290] [Citation(s) in RCA: 123] [Impact Index Per Article: 17.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Tobacco smoking is a known cause of gastric cancer, but several aspects of the association remain imprecisely quantified. We examined the relation between cigarette smoking and the risk of gastric cancer using a uniquely large dataset of 23 epidemiological studies within the 'Stomach cancer Pooling (StoP) Project', including 10 290 cases and 26 145 controls. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study-specific ORs using random-effects models. Compared with never smokers, the ORs were 1.20 (95% CI: 1.09-1.32) for ever, 1.12 (95% CI: 0.99-1.27) for former, and 1.25 (95% CI: 1.11-1.40) for current cigarette smokers. Among current smokers, the risk increased with number of cigarettes per day to reach an OR of 1.32 (95% CI: 1.10-1.58) for smokers of more than 20 cigarettes per day. The risk increased with duration of smoking, to reach an OR of 1.33 (95% CI: 1.14-1.54) for more than 40 years of smoking and decreased with increasing time since stopping cigarette smoking (P for trend<0.01) and became similar to that of never smokers 10 years after stopping. Risks were somewhat higher for cardia than noncardia gastric cancer. Risks were similar when considering only studies with information on Helicobacter pylori infection and comparing all cases to H. pylori+ controls only. This study provides the most precise estimate of the detrimental effect of cigarette smoking on the risk of gastric cancer on the basis of individual data, including the relationship with dose and duration, and the decrease in risk following stopping smoking.
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Affiliation(s)
- Delphine Praud
- Department of Clinical Sciences and Community Health, University of Milan
| | - Matteo Rota
- Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri, Milan
| | - Claudio Pelucchi
- Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri, Milan
| | - Paola Bertuccio
- Department of Clinical Sciences and Community Health, University of Milan
| | - Tiziana Rosso
- Department of Clinical Sciences and Community Health, University of Milan
| | - Carlotta Galeone
- Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri, Milan
| | - Zuo-Feng Zhang
- Department of Epidemiology, UCLA Fielding School of Public Health and Jonsson Comprehensive Cancer Center, Los Angeles, California
| | | | - Hidemi Ito
- Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, Japan
| | - Jinfu Hu
- Harbin Medical University, Harbin
| | - Kenneth C Johnson
- Department of Epidemiology and Community Health, University of Ottawa, Ottawa, Ontario
| | - Guo-Pei Yu
- Medical Informatics Center, Peking University, Peking, China
| | - Domenico Palli
- Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute - Istituto per lo Studio e la Prevenzione Oncologica (ISPO), Florence
| | - Monica Ferraroni
- Department of Clinical Sciences and Community Health, University of Milan
| | - Joshua Muscat
- The Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York
| | - Nuno Lunet
- EPIUnit - Institute of Public Health, University of Porto (ISPUP)
- Department of Clinical Epidemiology, Predictive Medicine and Public Health, University of Porto Medical School, Porto, Portugal
| | - Bárbara Peleteiro
- EPIUnit - Institute of Public Health, University of Porto (ISPUP)
- Department of Clinical Epidemiology, Predictive Medicine and Public Health, University of Porto Medical School, Porto, Portugal
| | - Reza Malekzadeh
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
| | - Weimin Ye
- Department of Medical Epidemiology and Biostatistics
| | - Huan Song
- Department of Medical Epidemiology and Biostatistics
| | - David Zaridze
- Department of Epidemiology and Prevention, Russian N.N. Blokhin Cancer Research Center, Moscow, Russia
| | - Dmitry Maximovitch
- Department of Epidemiology and Prevention, Russian N.N. Blokhin Cancer Research Center, Moscow, Russia
| | - Nuria Aragonés
- Environmental and Cancer Epidemiology Unit, National Center of Epidemiology, Instituto de Salud Carlos III
- CIBER Epidemiología y Salud Pública (CIBERESP)
- Cancer Epidemiology Research Group, Oncology and Hematology Area, IIS Puerta de Hierro, Madrid
| | - Gemma Castaño-Vinyals
- ISGlobal, Centre for Research in Environmental Epidemiology (CREAL)
- IMIM (Hospital del Mar Medical Research Institute)
- Universitat Pompeu Fabra (UPF), Barcelona
| | - Jesus Vioque
- ISGlobal, Centre for Research in Environmental Epidemiology (CREAL)
- Department of Public Health, Miguel Hernandez University, Campus San Juan, Alicante, Spain
| | - Eva M Navarrete-Muñoz
- ISGlobal, Centre for Research in Environmental Epidemiology (CREAL)
- Department of Public Health, Miguel Hernandez University, Campus San Juan, Alicante, Spain
| | - Mohammadreza Pakseresht
- Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Canada
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
- Nutritional Epidemiology Group, Centre for Epidemiology and Biostatistics, University of Leeds, Leeds
| | - Farhad Pourfarzi
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
- Department of Community Medicine, Ardabil University of Medical Sciences, Ardabil, Iran
| | - Alicja Wolk
- Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Nicola Orsini
- Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Andrea Bellavia
- Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Niclas Håkansson
- Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Lina Mu
- Department of Social and Preventive Medicine, School of Public Health and Health Professions, University at Buffalo, Buffalo
| | - Roberta Pastorino
- Section of Hygiene - Institute of Public Health, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario 'Agostino Gemelli'
| | - Robert C Kurtz
- Department of Medicine, Memorial Sloan Kettering Cancer Centre
| | - Mohammad H Derakhshan
- Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran
- Institute of Cardiovascular & Medical Sciences, University of Glasgow, Glasgow, UK
| | - Areti Lagiou
- Department of Public Health and Community Health, School of Health Professions, Athens Technological Educational Institute
| | - Pagona Lagiou
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
- Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece
| | - Paolo Boffetta
- The Tisch Cancer Institute, Mount Sinai School of Medicine, New York, New York
| | - Stefania Boccia
- Section of Hygiene - Institute of Public Health, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario 'Agostino Gemelli'
- ICAHN School of Medicine at Mount Sinai, New York, USA
- IRCCS SAN RAFFAELE PI SANA, Rome, Italy
| | - Eva Negri
- Department of Epidemiology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri, Milan
| | - Carlo La Vecchia
- Department of Clinical Sciences and Community Health, University of Milan
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16
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Ami R, Hatta W, Iijima K, Koike T, Ohkata H, Kondo Y, Ara N, Asanuma K, Asano N, Imatani A, Shimosegawa T. Factors Associated With Metachronous Gastric Cancer Development After Endoscopic Submucosal Dissection for Early Gastric Cancer. J Clin Gastroenterol 2017; 51:494-499. [PMID: 27505404 DOI: 10.1097/mcg.0000000000000620] [Citation(s) in RCA: 30] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
GOALS To clarify the factors associated with metachronous gastric cancer development after endoscopic submucosal dissection (ESD) for early gastric cancer. BACKGROUND Patients who undergo ESD for early gastric cancer have an appreciable risk of developing metachronous gastric cancer. However, there have been few reports on the association between life style and the development of such cancer. STUDY Patients with early gastric cancer who underwent ESD at our institution between 2003 and 2012 were enrolled. Metachronous gastric cancer was defined as secondary gastric cancer detected >1 year after initial ESD. Factors, including age, gender, body mass index, eradication of Helicobacter pylori, cigarette smoking, drinking, and continuous use of a proton pump inhibitor, associated with metachronous gastric cancer development were evaluated by Cox proportional hazard regression analysis. RESULTS A total of 539 patients with a mean 53.6-month follow-up period were analyzed. The 5-year cumulative incidence of secondary gastric cancer was 13.0%. Multivariate analysis exhibited that age of 60 years and above [hazard ratio (95% confidence interval)=4.05 (1.23-13.4)] and cigarette smoking [2.12 (1.19-3.78)] were independent risk factors for metachronous gastric cancer development. Furthermore, ≥20 pack-years of smoking [1.51 (1.03-2.24)] was a significant risk factor with a dose-response relationship (P for trend=0.042). There was no significant association between Helicobacter pylori eradication and metachronous gastric cancer development. CONCLUSIONS This is the first study to demonstrate the detailed association between cigarette smoking and metachronous gastric cancer development.
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Affiliation(s)
- Reiko Ami
- *Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai †Department of Gastroenterology, Akita University Graduate School of Medicine, Akita, Japan
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Park YM, Kim JH, Baik SJ, Park JJ, Youn YH, Park H. Clinical risk assessment for gastric cancer in asymptomatic population after a health check-up: An individualized consideration of the risk factors. Medicine (Baltimore) 2016; 95:e5351. [PMID: 27858920 PMCID: PMC5591168 DOI: 10.1097/md.0000000000005351] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/30/2022] Open
Abstract
For the prevention of gastric cancer, the detection of risk factors associated with precancerous conditions may be more informative. The aim of this study was to identify the risk factors of gastric cancer, including precancerous conditions: atrophic gastritis (AG), intestinal metaplasia (IM), and dysplasia.The clinical and endoscopic findings of 60,261 adults who underwent gastroduodenoscopy as part of a health check-up were reviewed retrospectively. Subgroup analysis was conducted according to age, sex, cancer stage, and histology based on Lauren classification.Gastric cancer was diagnosed in 75 patients (0.12%). Both IM and AG were independent risk factors for gastric cancer in all subgroups. Male, older age, obesity, diabetes mellitus (DM), a salty and spicy diet, and Helicobacter pylori (H. pylori) were significantly associated with precancerous conditions. However, risk factors related to precancerous conditions were different according to age and sex. In <40 years, H. pylori was the only risk factor related to precancerous conditions, whereas DM with a salty and spicy diet were additional risk factors in ≥40 years. In female individuals, obesity was significant risk factor for precancerous conditions as well as H. pylori infection.AG and IM are independent risk factors for gastric cancer. To prevent gastric cancer, H. pylori eradication may be more useful in <40 years, whereas additional factors such as DM, obesity, salty and spicy diet may be important in female or ≥40 years.
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Affiliation(s)
- Yoo Mi Park
- Department of Internal Medicine
- Health Promotion Center, Institute of Gastroenterology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
| | - Jie-Hyun Kim
- Department of Internal Medicine
- Correspondence: Jie-Hyun Kim, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, 211 Eonjuro, Gangnam-gu, Seoul, Korea (e-mail: )
| | - Su Jung Baik
- Health Promotion Center, Institute of Gastroenterology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
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Tan P, Yeoh KG. Genetics and Molecular Pathogenesis of Gastric Adenocarcinoma. Gastroenterology 2015; 149:1153-1162.e3. [PMID: 26073375 DOI: 10.1053/j.gastro.2015.05.059] [Citation(s) in RCA: 353] [Impact Index Per Article: 35.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/25/2015] [Revised: 05/18/2015] [Accepted: 05/20/2015] [Indexed: 02/07/2023]
Abstract
Gastric cancer (GC) is globally the fifth most common cancer and third leading cause of cancer death. A complex disease arising from the interaction of environmental and host-associated factors, key contributors to GC's high mortality include its silent nature, late clinical presentation, and underlying biological and genetic heterogeneity. Achieving a detailed molecular understanding of the various genomic aberrations associated with GC will be critical to improving patient outcomes. The recent years has seen considerable progress in deciphering the genomic landscape of GC, identifying new molecular components such as ARID1A and RHOA, cellular pathways, and tissue populations associated with gastric malignancy and progression. The Cancer Genome Atlas (TCGA) project is a landmark in the molecular characterization of GC. Key challenges for the future will involve the translation of these molecular findings to clinical utility, by enabling novel strategies for early GC detection, and precision therapies for individual GC patients.
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Affiliation(s)
- Patrick Tan
- Cancer and Stem Cell Biology Program, Duke-National University of Singapore Graduate Medical School, Singapore; Genome Institute of Singapore, Agency for Science, Technology, and Research, Singapore; Cancer Science Institute of Singapore, National University of Singapore, Singapore; Cellular and Molecular Research, National Cancer Centre Singapore, Singapore; Singapore Gastric Cancer Consortium, Singapore.
| | - Khay-Guan Yeoh
- Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Department of Gastroenterology and Hepatology, National University Health System, Singapore; Singapore Gastric Cancer Consortium, Singapore.
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Li LF, Chan RLY, Lu L, Shen J, Zhang L, Wu WKK, Wang L, Hu T, Li MX, Cho CH. Cigarette smoking and gastrointestinal diseases: the causal relationship and underlying molecular mechanisms (review). Int J Mol Med 2014; 34:372-80. [PMID: 24859303 DOI: 10.3892/ijmm.2014.1786] [Citation(s) in RCA: 140] [Impact Index Per Article: 12.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2014] [Accepted: 05/20/2014] [Indexed: 12/16/2022] Open
Abstract
Cigarette smoking is an important risk factor for gastrointestinal (GI) disorders, including peptic ulcers, inflammatory bowel diseases, such as Crohn's disease and cancer. In this review, the relationship between smoking and GI disorders and the underlying mechanisms are discussed. It has been demonstrated that cigarette smoking is positively associated with the pathogenesis of peptic ulcers and the delay of ulcer healing. Mechanistic studies have shown that cigarette smoke and its active ingredients can cause mucosal cell death, inhibit cell renewal, decrease blood flow in the GI mucosa and interfere with the mucosal immune system. Cigarette smoking is also an independent risk factor for various types of cancer of the GI tract. In this review, we also summarize the mechanisms through which cigarette smoking induces tumorigenesis and promotes the development of cancer in various sections of the GI tract. These mechanisms include the activation of nicotinic acetylcholine receptors, the formation of DNA adducts, the stimulation of tumor angiogenesis and the modulation of immune responses in the GI mucosa. A full understanding of these pathogenic mechanisms may help us to develop more effective therapies for GI disorders in the future.
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Affiliation(s)
- L F Li
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - R L Y Chan
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - L Lu
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - J Shen
- Institute of Digestive Diseases, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - L Zhang
- Institute of Digestive Diseases, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - W K K Wu
- Institute of Digestive Diseases, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - L Wang
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - T Hu
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - M X Li
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
| | - C H Cho
- School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, P.R. China
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Agudo A, Peluso M, Munnia A, Luján-Barroso L, Sánchez MJ, Molina-Montes E, Sánchez-Cantalejo E, Navarro C, Tormo MJ, Chirlaque MD, Barricarte A, Ardanaz E, Amiano P, Dorronsoro M, Quirós JR, Piro S, Bonet C, Sala N, González CA. Aromatic DNA adducts and risk of gastrointestinal cancers: a case-cohort study within the EPIC-Spain. Cancer Epidemiol Biomarkers Prev 2012; 21:685-92. [PMID: 22315368 DOI: 10.1158/1055-9965.epi-11-1205] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/28/2022] Open
Abstract
BACKGROUND Colorectal (CRC) and gastric cancer (GC) are associated with meat intake and tobacco smoke, maybe because of aromatic compounds occurring in tobacco smoking and formed during cooking meat. Activated metabolites of these compounds may bind to DNA forming bulky adducts. METHODS Forty-eight subjects diagnosed of GC and 154 of CRC during a 7-year follow-up period in the European Prospective Investigation into Cancer and Nutrition-Spain cohort were compared with a sample of 296 subjects using a case-cohort approach. Aromatic adducts to DNA from leukocytes collected at recruitment were measured by means of the (32)P-postlabeling technique. The relative risk (RR) and 95% confidence interval (CI), adjusted by relevant confounders were estimated by a modified version of Cox regression. RESULTS Using the log(2)-transformed adduct concentration, we observed a RR = 1.57 (CI: 1.25-1.97) for CRC, which means a 57% increased risk associated with doubling the level of adducts, and 47% (RR = 1.47, CI: 1.07-2.00) increase in risk of GC. The association was more marked for colon than for rectal tumors. CONCLUSIONS The level of aromatic adducts in the DNA is independently associated with an increased risk of gastric and CRCs. This effect could be due to aromatic compounds present in tobacco smoke or formed in meat, but they could be also due to genotoxic compounds from other sources. IMPACT Sources of aromatic compounds should be taken into account, in addition to known risk factors, in the research and prevention of tumors of the stomach, colon, and rectum.
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Affiliation(s)
- Antonio Agudo
- Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), Av. Gran Via 199-203, L'Hospitalet de Llobregat, Spain.
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Nomura AMY, Wilkens LR, Henderson BE, Epplein M, Kolonel LN. The association of cigarette smoking with gastric cancer: the multiethnic cohort study. Cancer Causes Control 2012; 23:51-8. [PMID: 22037905 PMCID: PMC4166441 DOI: 10.1007/s10552-011-9854-0] [Citation(s) in RCA: 56] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/18/2011] [Accepted: 10/04/2011] [Indexed: 12/30/2022]
Abstract
PURPOSE The purpose of this study is to investigate the association of cigarette smoking with gastric cancer. METHODS Over 215,000 men and women, representing five ethnic groups (African Americans, Japanese Americans, Latino Americans, Native Hawaiians, and Whites), completed a mailed questionnaire, 1993-1996. After an average follow-up of 7.3 years, 454 men and 242 women were diagnosed with gastric adenocarcinoma. Cox proportional hazard models were used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. RESULTS Current cigarette smokers had elevated hazard ratios compared with never smokers among men (HR = 1.98; 95% CI 1.46-2.70) and women (HR = 1.78; 95% CI 1.23-2.57). This positive association was consistent across all five ethnicities. Former smokers had an elevated risk among men, but not among women. There was a significant trend by intensity (cigarettes per day) and duration (years) of smoking among all current smokers. After separation by anatomic location of their tumor, ever smokers had a higher risk for gastric cardia cancer (HR = 2.86; 95% CI 1.66-4.93) than for distal gastric cancer (HR = 1.52; 95% CI 1.25-1.86) among men and women combined. Analysis by histologic tumor type showed a stronger association between current smoking and the intestinal type. CONCLUSIONS Overall, this study shows an association of current cigarette smoking with gastric cancer in both sexes, consistency of this effect across five ethnic groups, evidence for a dose-response effect of smoking in both sexes, a stronger effect for cardia than for distal gastric cancer, and a stronger association for intestinal than for diffuse gastric cancer.
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Affiliation(s)
- Abraham M Y Nomura
- Epidemiology Program, University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI 96813, USA.
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22
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Risk factors of precancerous gastric lesions in a population at high risk of gastric cancer. Chin J Cancer Res 2010. [DOI: 10.1007/s11670-010-0267-5] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022] Open
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Moy KA, Fan Y, Wang R, Gao YT, Yu MC, Yuan JM. Alcohol and tobacco use in relation to gastric cancer: a prospective study of men in Shanghai, China. Cancer Epidemiol Biomarkers Prev 2010; 19:2287-97. [PMID: 20699372 DOI: 10.1158/1055-9965.epi-10-0362] [Citation(s) in RCA: 98] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND Epidemiologic findings of tobacco and alcohol use in relation to gastric cancer are inconsistent. Well-designed prospective studies examining their relationship are sparse. METHODS The association between cigarette smoking/alcohol intake and gastric cancer risk was examined in a population-based prospective cohort of 18,244 middle-aged and older men in Shanghai, China, who were enrolled in the study during 1986-1989. After up to 20 years of follow-up, 391 incident gastric cancer cases were identified. Cox proportional hazards regression models were used to estimate hazard ratios (HR) and corresponding 95% confidence intervals (95% CI). RESULTS Ever smokers experienced a statistically significant increased risk of gastric cancer (HR, 1.59; 95% CI, 1.27-1.99) compared with nonsmokers after adjustment for alcohol intake and other confounders. Among nondrinkers, smokers experienced 80% increased risk of gastric cancer (HR, 1.81; 95% CI,1.36, 2.41). Conversely, heavy drinkers experienced a statistically significant increase in risk of gastric cancer (HR, 1.46; 95% CI, 1.05-2.04) among all subjects and a statistically nonsignificant 80% increased risk among never smokers. Further adjustment for Helicobacter pylori serology, serum levels of beta-carotene and vitamin C, and urinary level of total isothiocyanates in combination with glutathione S-transferase (GST) M1 and GSTT1 genotypes did not materially change the associations between smoking/alcohol consumption and gastric cancer risk. CONCLUSIONS These results suggest that cigarette smoking and alcohol consumption may exert independent effects on the development of gastric cancer in this high-risk population. IMPACT Modification of these lifestyle choices may reduce the incidence of gastric cancer.
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Affiliation(s)
- Kristin A Moy
- Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Masonic Cancer Center, Minneapolis, Minnesota 55455, USA.
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Shikata K, Doi Y, Yonemoto K, Arima H, Ninomiya T, Kubo M, Tanizaki Y, Matsumoto T, Iida M, Kiyohara Y. Population-based prospective study of the combined influence of cigarette smoking and Helicobacter pylori infection on gastric cancer incidence: the Hisayama Study. Am J Epidemiol 2008; 168:1409-15. [PMID: 18945691 DOI: 10.1093/aje/kwn276] [Citation(s) in RCA: 75] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
The authors assessed the separate and joint influences of cigarette smoking and Helicobacter pylori infection on the development of gastric cancer in a population-based prospective study. A total of 1,071 Japanese men aged > or =40 years were followed up prospectively for 14 years (1998-2002). Compared with that for current nonsmokers, the multivariate-adjusted hazard ratios of gastric cancer for smokers of 1-9, 10-19, and > or =20 cigarettes per day were 1.36 (95% confidence interval (CI): 0.50, 3.71), 1.93 (95% CI: 1.01, 3.67), and 1.88 (95% CI: 1.02, 3.43), respectively. The risk of gastric cancer increased steeply for subjects who had both a smoking habit and H. pylori infection compared with those who did not have both risk factors (hazard ratio = 11.41, 95% CI: 1.54, 84.67). If causal, the estimated population attributable fraction of gastric cancer for cigarette smoking was approximately half that for H. pylori infection (28.4% vs. 56.2%). The overlap of the population attributable fractions for the 2 factors was 49.6%. Findings suggest that cigarette smoking and H. pylori infection are significant risk factors for gastric cancer in Japanese men, and the magnitude of their combined influence is considerable.
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Affiliation(s)
- Kentaro Shikata
- Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
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Kim Y, Shin A, Gwack J, Jun JK, Park SK, Kang D, Shin HR, Chang SH, Yoo KY. Cigarette Smoking and Gastric Cancer Risk in a Community-based Cohort Study in Korea. J Prev Med Public Health 2007; 40:467-74. [DOI: 10.3961/jpmph.2007.40.6.467] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Affiliation(s)
- Yeonju Kim
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Aesun Shin
- Division of Cancer Prevention, National Cancer Control Research Institute, National Cancer Center, Goyang, Korea
| | - Jin Gwack
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Jae Kwan Jun
- Division of Cancer Prevention, National Cancer Control Research Institute, National Cancer Center, Goyang, Korea
| | - Sue Kyung Park
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Daehee Kang
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
| | - Hai-Rim Shin
- Division of Cancer Prevention, National Cancer Control Research Institute, National Cancer Center, Goyang, Korea
| | - Soung-Hoon Chang
- Department of Preventive Medicine, Konkuk University College of Medicine, Chungju, Korea
| | - Keun-Young Yoo
- Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea
- National Cancer Center, Goyang, Korea
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Shen J, Wang RT, Xu YC, Wang LW, Wang XR. Interaction models of CYP1A1, GSTM1 polymorphisms and tobacco smoking in intestinal gastric cancer. World J Gastroenterol 2005; 11:6056-60. [PMID: 16273625 PMCID: PMC4436735 DOI: 10.3748/wjg.v11.i38.6056] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To explore the interaction models of the cytochrome P-450 (CYP) 1A1 Val variant and glutathione S-transferase (GST) M1 null polymorphisms with tobacco smoking in the occurrence of intestinal gastric cancer.
METHODS: A community-based case-control study was conducted in Yangzhong. Subjects included 114 intestinal types of gastric cancer with endoscopic and pathological diagnosis during January 1997 and December 1998, and 693 controls selected from their spouse, siblings or siblings-in-law who had no history of digestive system cancer. Logistic regression was used to estimate the interaction models.
RESULTS: The frequency of the CYP1A1 Val variant allele in cases did not differ from that in controls. The OR of GSTM1 null genotype was 2.0 (95% confidence interval [95%CI]: 1.2-3.1, P<0.01). It showed a significant type 2 form of interaction model when both CYP1A1 Valvariant allele and former tobacco smoking existed (i.e., among the multiplicative effects, the disease risk is increased by the tobacco exposure alone but not by the CYP1A1 variant alone). The interaction index g was 2.8, and OReg(95%CI) was 5.0 (1.9-13.4). GSTM1 null genotype and former tobacco smoking were significant in a type 4 interaction model (i.e., the disease risk is increased by GSTM1 null genotype or tobacco exposure alone among the multiplicative effects). The interaction index g and OReg (95%CI) were 3.4 and 8.4 (3.4-20.9), respectively.
CONCLUSION: Different interaction models of CYP1A1 Val variant allele and GSTM1 null genotype with tobacco smoking will contribute to understanding carcinogenic mechanism, but there is a need to further investigate in larger scale studies.
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Affiliation(s)
- Jing Shen
- Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 701 West 168th Street (Room 505), New York, NY 10032, USA.
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Environmental Factors in Helicobacter pylori-Related Gastric Precancerous Lesions in Venezuela. Cancer Epidemiol Biomarkers Prev 2004. [DOI: 10.1158/1055-9965.468.13.3] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
Abstract
Although Helicobacter pylori (HP) infection has been acknowledged to play an etiological role in gastric carcinogenesis, its relatively weak association particularly in developing countries suggests critical roles of cofactors. Among a population with an extremely high prevalence of HP infection (≈95%) in Venezuela, we examined the relationship of household characteristics, smoking, alcohol drinking, dietary consumption, and plasma nutrient levels with the prevalence of three different stages of gastric precancerous lesions, chronic atrophic gastritis (AG; n = 337), intestinal metaplasia (IM; n = 551), and dysplasia (n = 157), in comparison with those without any of these lesions (n = 1154). Length of refrigerator use was marginally inversely associated with the prevalence of the precursor lesions studied. The association was most pronounced for AG followed by dysplasia. On the other hand, smoking status was a significant predictor for IM and dysplasia. Those smoking ≥10 cigarettes/day had 1.8-fold risk of IM and 3.6-fold risk of dysplasia compared with never smokers. There were no associations with alcohol consumption. When six food groups known to be associated with stomach cancer risk in Venezuela were tested, the prevalence of these lesions progressively increased with increasing starchy vegetable consumption and decreasing fresh fruit/fruit juice consumption. The association with fruits was more evident for dysplasia and AG and that with starchy vegetables for IM and AG. However, there were no inverse associations with plasma antioxidant vitamins. These findings offer important public health implications in preventing progression of HP-associated gastric precancerous lesions in high-risk populations.
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Abdul-Momen M, Monden Y, Hamada K, Komaki K, Kondo K, Umemoto A. DNA adducts detected in human gastric mucosa. CANCER DETECTION AND PREVENTION 2003; 27:209-15. [PMID: 12787728 DOI: 10.1016/s0361-090x(03)00065-5] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
Human gastrointestinal neoplasms are mostly developed from the mucosa, not from the adjacent muscle layer. DNA adducts in the mucosa and adjacent muscle layer of the non-tumoral part of stomach from 19 patients with gastric neoplasms and from six newborns were analyzed by 32P-postlabeling, and then compared them with those of representative colon or small intestine sample. Five kinds of mucosa-specific DNA adducts (G1-5) were found in all of the adult stomach samples, but were entirely absent from the adjacent muscle layers and from the newborn stomachs. In addition, several common background adducts were also present in both the mucosa and muscle layer. G2 was the same DNA adduct as Si2 in the small intestine and C1 in the colon, and G3 was the same as Si1 in the small intestine. Thus, it was demonstrated that the mucosa of the stomach was exposed to DNA-reactive substances.
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Affiliation(s)
- Mohammed Abdul-Momen
- Second Department of Surgery, School of Medicine, University of Tokushima, 3-18-15, Kuramoto-cho, Tokushima 770-8503, Japan
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González CA, Pera G, Agudo A, Palli D, Krogh V, Vineis P, Tumino R, Panico S, Berglund G, Simán H, Nyrén O, Agren A, Martinez C, Dorronsoro M, Barricarte A, Tormo MJ, Quiros JR, Allen N, Bingham S, Day N, Miller A, Nagel G, Boeing H, Overvad K, Tjonneland A, Bueno-De-Mesquita HB, Boshuizen HC, Peeters P, Numans M, Clavel-Chapelon F, Helen I, Agapitos E, Lund E, Fahey M, Saracci R, Kaaks R, Riboli E. Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC). Int J Cancer 2003; 107:629-34. [PMID: 14520702 DOI: 10.1002/ijc.11426] [Citation(s) in RCA: 159] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking.
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Affiliation(s)
- Carlos A González
- Department of Epidemiology, Catalan Institute of Oncology, Barcelona, Spain.
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Chao A, Thun MJ, Henley SJ, Jacobs EJ, McCullough ML, Calle EE. Cigarette smoking, use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II. Int J Cancer 2002; 101:380-9. [PMID: 12209964 DOI: 10.1002/ijc.10614] [Citation(s) in RCA: 107] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.
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Affiliation(s)
- Ann Chao
- Epidemiology and Surveillance Research, American Cancer Society, Atlanta, GA 30329-4251, USA.
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Besaratinia A, Besarati Nia A, Kleinjans JCS, Van Schooten FJ. Biomonitoring of tobacco smoke carcinogenicity by dosimetry of DNA adducts and genotyping and phenotyping of biotransformational enzymes: a review on polycyclic aromatic hydrocarbons. Biomarkers 2002; 7:209-29. [PMID: 12141065 DOI: 10.1080/13547500110120000] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/16/2022]
Abstract
In this review article, we summarize the data on tobacco smoke carcinogenicity in relation to DNA adduct dosimetry and genotyping and phenotyping of biotransformational enzymes. A major class of carcinogens, polycyclic aromatic hydrocarbons, present in substantial quantities in tobacco smoke, is discussed. The historical background and an overview of the metabolic pathways are given. The epidemiological and biological data in particular on dosimetry of the representative DNA adducts and genotyping and phenotyping of the respective activating and detoxifying enzymes are presented. The salient findings are highlighted, the uncertainties are underlined and, finally, recommendations for future research are made.
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Affiliation(s)
- A Besaratinia
- Department of Biology, Beckman Research Institute of the City of Hope, 1450 East Duarte Road, Duarte, CA 91010-3000, USA.
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Abstract
Few studies have provided information on the role of smoking and alcohol in the carcinogenesis of gastric cancer by sub-site and histologic type. The relationship of snuff dipping with risk of gastric cancer has also been rarely studied. In a population-based case-control study conducted in 5 counties of Sweden from February 1989 to January 1995, a total of 90 cases of gastric cardia cancer, 260 and 164 cases of distal gastric cancer of intestinal and diffuse types, respectively, and 1164 frequency-matched control subjects were personally interviewed about life-time smoking, use of smokeless tobacco and use of alcohol 20 years ago. Current smokers had a higher risk than never-smokers for all 3 kinds of gastric adenocarcinoma [odds ratio (OR) 1.7, 95% confidence interval (CI) 1.0-3.1 for gastric cardia adenocarcinoma; OR 1.8, 95% CI 1.2-2.7 for distal gastric cancer of intestinal type; and OR 2.2, 95% CI 1.4-3.5 for distal gastric cancer of diffuse type], and the risk rose with increasing dose and duration of smoking among current smokers. However, no elevated risk was observed for ex-smokers. Neither intake of alcoholic beverages nor snuff dipping was associated with an increased risk of any type of cardia or gastric cancer. Our study did not support the hypothesis that the role of tobacco differs by sub-site and histologic sub-type of gastric cancer.
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Affiliation(s)
- W Ye
- Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden.
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Wong BCY, Lam SK. Epidemiology of gastric cancer in relation to diet and Helicobacter pylori infection. J Gastroenterol Hepatol 1998; 13:S166-S172. [PMID: 28976648 DOI: 10.1111/j.1440-1746.1998.tb01871.x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
Gastric cancer is the second most common fatal malignancy in the world. In China, gastric cancer is now the second most common malignancy, while in Hong Kong, the mortality rate ranked fourth among all cancers in 1995. Dietary factors in gastric carcinogenesis came mostly from case-control studies. N-Nitroso compounds from dietary sources such as preserved, smoked and salted foods were found to be associated with gastric cancer. ß-Carotene, selenium and α-tocopherol have been shown in an intervention study to be favourable in the reduction of stomach cancer mortality. Fruits and vegetables showed the most consistent results of inverse association with gastric cancer. Dietary salt intake in preserved or salted foods is also shown to be associated with gastric cancer. Tea drinking, especially green tea, has a protective effect against gastric cancer as shown in some studies. Prospective case-control studies of the association between Helicobacter pylori infection and the subsequent development of gastric cancer showed that the odds ratio ranged from 2.8 to 6.0. However, results of similar case-control studies in countries with a high frequency of gastric cancer are controversial. Infection with H. pylori leads to changes in the vitamin C content of gastric juice, reactive oxygen metabolites, epithelial cell proliferation and apoptosis. Recently, CagA-positive strains were found to be associated with gastric cancer and also duodenal ulcers. The exact role of H. pylori in gastric carcinogenesis is still under investigation. Large-scale intervention studies are underway to examine dietary supplementation, H. pylori infection and gastric cancer. Helicobacter pylori eradication for gastric cancer prevention is being conducted in China and other parts of the world. In high-risk areas, for example in China, a combination approach including H. pylori eradication and dietary supplementation may be necessary.
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Affiliation(s)
| | - Shiu-Kum Lam
- Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong
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Lee BM, Jang JJ, Kim HS. Benzo[a]pyrene diol-epoxide-I-DNA and oxidative DNA adducts associated with gastric adenocarcinoma. Cancer Lett 1998; 125:61-68. [PMID: 9566697 DOI: 10.1016/s0304-3835(97)00520-x] [Citation(s) in RCA: 57] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BPDE-I-DNA and oxidative DNA adducts (8-OHdG) were investigated in stomach tissues (tumor and tumor-adjacent) of patients (N = 211) with gastric adenocarcinoma and in normal stomach tissues (N = 113). In each stomach specimen, the levels of BPDE-I-DNA adducts were quantitatively measured by enzyme linked immunosorbent assay (ELISA) and oxidative DNA damage was measured by HPLC-ECD. Higher levels of total BPDE-I-DNA adduct were observed in tumor (4.20 +/- 0.59 fmol/microg DNA) and tumor-adjacent (3.68 +/- 0.62 fmol/microg DNA) tissues than in normal stomach tissues (2.80 +/- 0.53 fmol/microg DNA) but were not significant. In males, BPDE-I-DNA adduct was significantly higher in tumor tissues (4.25 +/- 0.42 fmol/microg DNA) than in normal tissues (2.83 +/- 0.59 fmol/microg DNA) (P < 0.05). In smokers, BPDE-I-DNA adduct was slightly higher in tumor tissues (4.92 +/- 0.82 fmol/microg DNA) than in tumor-adjacent tissues (3.99 +/- 0.92 fmol/microg DNA). Gastric cancer patients had significantly higher levels of 8-OHdG in their tumor-adjacent (7.54 +/- 0.43 residues/10(5) dG) and tumor tissues (6.29 +/- 0.39 residues/10(5) dG) than in normal tissues (2.86 +/- 0.11 residues/10(5) dG) (P < 0.001). Smokers showed higher levels of 8-OHdG in both tumor (6.44 +/- 0.62 residues/10(5) dG) and tumor-adjacent (8.12 +/- 0.68 residues/10(5) dG) tissues than in non-smokers (5.80 +/- 0.47 and 7.11 +/- 0.57 residues/10(5) dG, respectively). 8-OHdG levels were significantly increased in positive tissues with Helicobacter pylori (H. pylori) infection compared with negative tissues (P < 0.01). Also, the frequency of H. pylori infection was higher in tumor-adjacent tissues (73%) than in tumor (42%) or normal tissues (44%). These results demonstrate that there are higher levels of 8-OHdG and BPDE-I-DNA adducts in tumor and tumor-adjacent tissues than in normal tissues and that these higher levels might be related to gastric tumorigenesis, although benzo[a]pyrene could be a minor contributing component in the environment.
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Affiliation(s)
- B M Lee
- Division of Toxicology, College of Pharmacy, Sung Kyun Kwan University, Suwon, South Korea.
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35
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Abstract
Although declining, gastric cancer (GC) is estimated to be second in frequency worldwide. Major causes appear to be environmental rather than genetic. A relationship has been suggested between tobacco smoking and GC. A number of epidemiological studies have been performed dealing with this question. All the cohort studies showed a significantly increased risk of GC of the order of 1.5-2.5 for cigarette smokers. Evidence from case-control studies is less consistent. We have carried out a meta-analysis on the 40 studies providing a quantitative estimate of the association between GC risk and tobacco smoking. Results suggest a risk of stomach cancer among smokers of the order of 1.5-1.6 as compared to non-smokers. The summary relative risk was higher in men (1.59) than in women (1.11). Several studies examined the dose-response relationship which existed in 4 cohort studies and 6 case-control studies. We estimated the number of GC cases attributable to tobacco smoking occurring worldwide: in total, over 80,000 cases of GC (11% of all estimated cases) may be attributed to tobacco smoking each year. This figure is larger than that estimated for other cancers for which association with tobacco smoking is clearly established, such as pancreatic and renal cancers.
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Affiliation(s)
- J Trédaniel
- Unit of Environmental Cancer Epidemiology, International Agency for Research on Cancer, Lyon, France
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Abstract
In contrast to acute or chronic dosing experiments with a single chemical in animals, man is exposed to thousands of chemicals during a lifetime. Each of these may act alone, additively, synergistically or antagonistically in terms of biological effects, but most current risk assessment procedures fail to recognize such interactions. In carcinogenesis, a mutational process that is thought to occur through DNA damage by endogenous and/or exogenous agents, a wide variety of host factors is involved in disease outcome. These include absorption of chemicals, their distribution, metabolism and excretion. In addition, once metabolic activation has occurred, there is an array of protective mechanisms that cells have evolved to maintain DNA integrity, such as DNA repair, genetic redundancy and programmed cell death. One approach to risk assessment is to regard all DNA-damaging events as potentially leading to cancer and to measure DNA damage as the biologically relevant endpoint. The main method, if not the only method, presently available to assay a wide range of DNA adducts is 32P-postlabelling. This method has high sensitivity (limit of detection > 1 adduct per 10(10) nucleotides) and is capable of visualizing many different DNA adducts in a single analysis. Postlabelling is best suited for detecting hydrophobic adducts--low molecular weight adducts usually need a preliminary separation procedure prior to being postlabelled. This chromatographic procedure has been used to study DNA samples from human tissues of cigarette smokers, occupationally exposed groups and individuals living in polluted environments. Correlations have been found between the severity of exposure and the level of DNA adducts detected for human samples. However, most studies are single-time point studies, whereas for risk assessment purposes it may be better to use more quantitative and representative measures of long-term exposure, for example the number of adducts formed per annum. This article reviews methods of DNA adduct measurement, with particular reference to the 32P-postlabelling technique, which has been used to determine DNA adduct levels in populations exposed to complex mixtures.
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Affiliation(s)
- C M Dale
- Department of Biology, University of York, Heslington, UK
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Hansson LE, Baron J, Nyrén O, Bergström R, Wolk A, Adami HO. Tobacco, alcohol and the risk of gastric cancer. A population-based case-control study in Sweden. Int J Cancer 1994; 57:26-31. [PMID: 8150537 DOI: 10.1002/ijc.2910570106] [Citation(s) in RCA: 68] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
Previous studies have provided conflicting information on the role of tobacco and alcohol in gastric carcinogenesis. A population-based case-control study with 338 histologically confirmed gastric-cancer cases and 679 control subjects was conducted. Information relating to life-time tobacco consumption, alcohol intake and diet during adolescence and 20 years before interview, and to socio-economic conditions was obtained through face-to-face interviews. Current cigarette smokers were found to have a greater risk than non-users of tobacco. The duration of cigarette or pipe smoking was positively associated with gastric-cancer risk. There was significant interaction between tobacco use and fruit consumption. High fruit intake was more protective among users of tobacco than among non-users, and the risk estimates associated with cigarette smoking were higher among those with low fruit consumption than among frequent fruit-eaters. Likewise, though to a lesser extent, vegetable intake interacted with tobacco use. Snuff dipping and alcohol intake was not associated with gastric-cancer risk. However, high alcohol intake tended to increase the risk associated with tobacco use. This study adds further support to the role of tobacco smoking in gastric carcinogenesis, and demonstrates that high intake of fruits and vegetables may be particularly beneficial in smokers.
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Affiliation(s)
- L E Hansson
- Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden
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Dyke GW, Craven JL, Hall R, Garner RC. DNA damage as measured by 32P-postlabelling in normal and pre-malignant gastric mucosa. Cancer Lett 1994; 77:45-50. [PMID: 8162561 DOI: 10.1016/0304-3835(94)90346-8] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
DNA was extracted from the gastric mucosa of 69 patients and analysed for the presence of DNA adducts by 32P-postlabelling. Adduct levels found in patients with histologically normal gastric mucosa were compared with levels found in patients displaying evidence of chronic atrophic gastritis or intestinal metaplasia, both of which may be considered pre-malignant conditions. Adduct patterns were the same for all patients, but the highest adduct levels were found in the latter two groups. Mean adduct levels were also higher in patients with abnormal gastric mucosa, but there was no statistically significant difference in adduct levels between the normal and pre-malignant groups (P > 0.05, Mann-Whitney U test). Thus DNA adduct levels do not correlate with the presence of histological abnormalities in the stomach and are not useful as a marker of malignant potential.
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Affiliation(s)
- G W Dyke
- Jack Birch Unit for Environmental Carcinogenesis, University of York, UK
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40
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Shaw GR, Connell DW. Prediction and monitoring of the carcinogenicity of polycyclic aromatic compounds (PACs). REVIEWS OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY 1994; 135:1-62. [PMID: 8171214 DOI: 10.1007/978-1-4612-2634-5_1] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/22/2023]
Abstract
Chemical carcinogenesis is a multistage process that includes initiation, promotion, and progression. Some carcinogenic PACs have been shown to activate proto-oncogenes and deactivate tumor-suppression genes in the carcinogenic process. The function of DNA repair processes appears to be changed in some cases by PACs. Many PACs are well known for their carcinogenic activity, but for this activity to be exerted, metabolic activation by microsomal enzymes must occur. The enzyme system responsible for PAC activation is the mixed-function oxidase system and, in particular, cytochrome P-450. In the case of PAHs, oxidation predominantly produces reactive diol-epoxides that can then be converted to carbonium ions as the reactive electrophiles that can then covalently bind to DNA. Regions of high activity exist in PAHs, namely, the "bay," "K," and "L" regions which are associated with pi electron distribution. The diol-epoxides can exist in either syn or anti forms, each of which has two enantiomers producing four stereoisomers in all. Energy considerations favor the formation of the anti form. Nitrogen-containing PACs can be metabolically activated in a manner similar to that for PAHs, or the nitrogen atom can be oxidized to form hydroxylamines. These reactive electrophiles can then form covalently bound DNA adducts. The monitoring of DNA adducts has been used in risk assessment for human exposure to PACs. This form of biomonitoring has advantages over the monitoring of external exposure or body levels of the chemicals in question. In the case of PACs, binding to DNA is an important step in the multistage carcinogenic process. The estimation of DNA adducts has been used in the monitoring of humans exposed to PAHs in a wide range of industrial situations. Recent research has shown a dose-response relationship between PAH adduct levels and human cancer, thus developing molecular epidemiology as a relevant science for the field of risk assessment. Techniques have been developed for the determination of DNA adducts and these include immunochemical, fluorescence spectroscopic, GC-MS, and 32P-postlabeling methods. The 32P-postlabeling assay is by far the most sensitive, with limits of detection being of the order of one adduct in 10(10) normal nucleotides. The use of HPLC for separation of adducted nucleotides in this postlabeling assay is becoming more common and gives better resolution of adducts than does the TLC technique used in the traditional assay. The detection of adducts on hemoglobin and other proteins has been used as a surrogate for DNA adduct estimation.(ABSTRACT TRUNCATED AT 400 WORDS)
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Affiliation(s)
- G R Shaw
- National Research Centre for Environmental Toxicology, Queensland, Australia
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41
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Abstract
This study analysed gastric mucosal DNA by 32P-postlabelling in a series of patients who have had previous vagotomy for benign peptic ulcer disease. DNA adduct levels were found to be significantly higher in patients who had had previous truncal vagotomy than in those who had had previous highly selective vagotomy (p < 0.001). Intragastric bile concentrations were also considerably higher in patients after truncal vagotomy but there was no correlation between intragastric bile concentrations and DNA adduct levels. These results suggest that, although duodenogastric reflux may be a cause of gastric mucosal DNA damage in the stomach after vagotomy, measurement of total intragastric bile does not accurately reflect genotoxic insult.
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Affiliation(s)
- G W Dyke
- Jack Birch Unit for Environmental Carcinogenesis, Department of Biology, University of York
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