Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

Peleteiro, Bárbara; Castro, Clara; Morais, Samantha; Ferro, Ana; Lunet, Nuno

doi:10.1007/s10620-015-3624-x

Cited by 39 publications

(27 citation statements)

References 32 publications

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“…Our OR estimates for current cigarette smokers were, if anything, slightly lower than those on the basis of published studies, which found risks ranging between 1.5 and 1.7 (Tredaniel et al, 1997; Ladeiras-Lopes et al, 2008; La Torre et al, 2009;Bonequi et al, 2013), resulting in an estimated worldwide population attributable fraction of 19.5% in men and 3.0% in women (Peleteiro et al, 2015). Publication bias may have led to an overestimation of the risk in the published literature.…”

Section: Discussioncontrasting

confidence: 82%

Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project

Praud

Rota

Pelucchi

et al. 2018

European Journal of Cancer Prevention

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162

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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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Section: Discussioncontrasting

confidence: 82%

Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project

Praud

Rota

Pelucchi

et al. 2018

European Journal of Cancer Prevention

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162

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“…It was previously reported that smokers had higher levels of DOUX2 expression in the tracheal and airway epithelium than nonsmokers [ 34 ]. Smoking is a contributing factor of the carcinogenesis of gastric cancer [ 31 , 35 ]. Recently it has been reported that smoking suppresses regulatory B cell and inhibits the production of interleukin 10; both events may increase the risk of gastric cancer [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

DUOX2 Expression Is Increased in Barrett Esophagus and Cancerous Tissues of Stomach and Colon

Zhou

et al. 2016

Gastroenterology Research and Practice

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Aim. To detect the expression of dual oxidase (DUOX) 2 in Barrett esophagus, gastric cancer, and colorectal cancer (CRC). Materials and Methods. The endoscopic biopsies were collected from patients with Barrett esophagus, while the curative resection tissues were obtained from patients with gastric cancer, CRC, or hepatic carcinoma. The DUOX2 protein and mRNA levels were detected with immunohistochemistry (IHC) and real-time quantitative PCR (qPCR). The correlation of DUOX2 expression with clinicopathological parameters of tumors was identified. Results. Low levels of DUOX2 mRNA were detected in Barrett esophagus and the adjacent normal tissues, and there was no difference between these two groups. DUOX2 protein was found in Barrett esophagus and undetectable in the normal epithelium. The DUOX2 mRNA and protein levels in the gastric cancer and CRC were increased compared to the adjacent nonmalignant tissues. The elevated DUOX2 in the gastric cancer was significantly associated with smoking history. In CRC tissues, the DUOX2 protein expression level in stages II–IV was significantly higher than that in stage I. In both hepatic carcinoma and the adjacent nonmalignant tissue, the DUOX2 was virtually undetectable. Conclusion. DUOX2 in Barrett esophagus, gastric cancer, and CRC may be involved in the tumorigenesis of these tissues.

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“…H. pylori is now well known to be linked to stomach cancer in many studies along with EBV [14–18]. Other risk factors for GC include chronic gastritis [9], older age [19], male sex [20, 21], a diet high in salt [22–24], smoking [25, 26], alcohol consumption [27], poorly preserved foods [28], diet low in fruits and vegetables [29], tobacco product [30], pernicious anaemia [31–33], a history of stomach surgery for benign conditions [34], and a family history of stomach cancer [34, 35]. …”

Section: Introductionmentioning

confidence: 99%

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

Singh

Jha

2017

Journal of Oncology

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Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.

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Worldwide Burden of Gastric Cancer Attributable to Tobacco Smoking in 2012 and Predictions for 2020

Abstract: Smoking accounts for a larger number of gastric cancer cases among men, and gender differences are expected to increase in the next decade, despite the decrease in PAFs. Intensified efforts to control smoking are needed to further reduce the burden of gastric cancer.

Cited by 39 publications

References 32 publications

Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project

Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project

DUOX2 Expression Is Increased in Barrett Esophagus and Cancerous Tissues of Stomach and Colon

Status of Epstein-Barr Virus Coinfection withHelicobacter pyloriin Gastric Cancer

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