Association of interleukin-1β –511 C/T polymorphism with tobacco-associated cancer in northeast India: a study on oral and gastric cancer

Lakhanpal, Meena; Yadav, Devendra Kumar; Devi, Thoudam Regina; Singh, Laishram Chandreshwor; Singh, Khangembam Jitenkumar; S, Latha; Chauhan, Pradeep S.; Verma, Yogesh Kumar; Zomavia, Eric; Sharma, Jagannath Dev; Kataki, Amal Chandra; Saxena, Sunita; Kapur, Sujala

doi:10.1016/j.cancergen.2014.01.002

Cited by 25 publications

(14 citation statements)

References 43 publications

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“…Another meta-analysis found that, except in cases of very heavy drinking, alcohol was not strongly associated with gastric cancer [ 35 ]. Few studies have discussed the relationship between betel quid chewing and gastric cancer and the results were inconsistent [ 21 , 36 ]. Our previous case-control study found betel quid to be a significant risk factor for gastric cancer [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of alcohol consumption, cigarette smoking, and betel quid chewing on upper digestive diseases: a large cross-sectional study and meta-analysis

Chuang

et al. 2017

Oncotarget

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Cigarette smoking is a well-known risk factor of upper digestive diseases. Findings on alcohol's effect on these diseases are inconsistent and with the exception of its association with esophageal cancer, little is known about betel quid chewing. This study investigated the association between use of these three substances and upper digestive diseases. We collected data from 9,275 patients receiving upper endoscopies between April 2008 and December 2013. Polynomial regressions were used to analyze the association between risk factors and diseases of the esophagus, stomach and duodenum. Meta-analysis for use of these substances and esophageal diseases was also performed. Participants who simultaneously consumed cigarettes, alcohol and betel quid had a 17.28-fold risk of esophageal cancer (95% CI = 7.59–39.33), 2.99-fold risk of Barrette's esophagus (95% CI = 2.40–4.39), 1.60-fold risk of grade A-B erosive esophagitis (95% CI = 1.29–2.00), 2.00-fold risk of gastric ulcer (95% CI = 1.52–2.63), 2.12-fold risk of duodenitis (95% CI = 1.55–2.89) and 1.29-fold risk of duodenal ulcer (95% CI = 1.01–1.65). Concurrent consumption of more substances was associated with significantly higher risk of developing these diseases. Meta-analysis also revealed use of the three substances came with a high risk of esophageal diseases. In conclusions, cigarette smoking, alcohol drinking and betel quid chewing were associated with upper digestive tract diseases.

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Section: Discussionmentioning

confidence: 99%

Effects of alcohol consumption, cigarette smoking, and betel quid chewing on upper digestive diseases: a large cross-sectional study and meta-analysis

Chuang

et al. 2017

Oncotarget

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“…CT+TT p=0.02 [43] rs189037 (ATM) AA p=3.71*10-6 [31] rs187238 (IL-18) GC p=0.003 [44] rs34329 (p27) GG p<0.0001 [32] rs1800625 (RAGE) TC p<0.05 ;…”

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confidence: 99%

Single Nucleotide Polymorphisms and Risk of Oral Cancer: Indian Case-Control Study

Multania¹,

Saranath²

2016

J Clin Cell Immunol

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“…A meta-analysis on IL-1β-31C/T summarized that the T allele was associated with increased risk of GC only in Asians (allele C vs allele T: OR: 0.86; 95% CI: 0.73-0.98; I 2 = 1.8%), and H. pylori infection could enhance the risk even more (allele C vs allele T: OR: 0.76; 95% CI: 0.61-0.96; I 2 =2.6%) (table 1) [9]. This conclusion should be updated as this meta-analysis only included studies from 1990 to 2006, and many studies have been published since then [25,28,[35][36][40][41][42][43][44][45][46][47][48][49][50]. A very recent meta-analysis reported similar correlation where the T/T genotype of IL-1β-31 increased GC risk only in individuals with H. pylori infection (table 1) [51].…”

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confidence: 91%

Interaction Between Helicobacter Pylori and Host Genetic Variants in Gastric Carcinogenesis

et al. 2016

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Helicobacter pylori (H. pylori) is the definite carcinogen of gastric cancer. H. pylori infection induces chronic inflammation, causes DNA damage and aberrant methylation of genes and these pathways are involved in H. pylori-related gastric carcinogenesis. Polymorphisms of the genes involved in these pathways could alter susceptibility to gastric cancer. In this mini review, we focused on the role of polymorphisms in these genes on the susceptibility to gastric cancer, with a particular emphasis on their possible interactions with H. pylori infection. We found that many studies on this theme did not simultaneously report H. pylori infection and the interactions remained inconclusive.

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Association of interleukin-1β –511 C/T polymorphism with tobacco-associated cancer in northeast India: a study on oral and gastric cancer

Cited by 25 publications

References 43 publications

Effects of alcohol consumption, cigarette smoking, and betel quid chewing on upper digestive diseases: a large cross-sectional study and meta-analysis

Effects of alcohol consumption, cigarette smoking, and betel quid chewing on upper digestive diseases: a large cross-sectional study and meta-analysis

Single Nucleotide Polymorphisms and Risk of Oral Cancer: Indian Case-Control Study

Interaction Between Helicobacter Pylori and Host Genetic Variants in Gastric Carcinogenesis

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