CYP2E1 Genetic Polymorphism with Dietary, Tobacco, Alcohol Habits, H. pylori Infection Status and Susceptibility to Stomach Cancer in Mizoram, India

Malakar, M. C.; Devi, Kangjam Rekha; Phukan, Rup Kumar; Kaur, Tanvir; Deka, Manab; Puia, Lalhriat; Baruah, Debajit; Mahanta, Jagadish; Narain, Kanwar

doi:10.7314/apjcp.2014.15.20.8815

Cited by 10 publications

(8 citation statements)

References 37 publications

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“…Few studies showed a significant association of CYP2E1 RsaI polymorphism with stomach cancer risk [196,197], while others found no association [186,[198][199][200]. Recently, a study in an Indian population also found no role of CYP2E1 RsaI polymorphism in predisposition to stomach cancer [201].…”

Section: Stomach/gastric Cancermentioning

confidence: 97%

Cytochrome P450 in Cancer Susceptibility and Treatment

Mittal

Tulsyan

Kumar

et al. 2015

Advances in Clinical Chemistry

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Section: Stomach/gastric Cancermentioning

confidence: 97%

Cytochrome P450 in Cancer Susceptibility and Treatment

Mittal

Tulsyan

Kumar

et al. 2015

Advances in Clinical Chemistry

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“…Tobacco smoke is an important risk factor for gastric cancer. Studies have revealed the positive link between tobacco smoke and risk of gastric cancer initiation and development [ 7 , 8 , 9 , 10 , 11 , 12 ]. Many ingredients found in tobacco smoke are known to induce free radicals and possess toxic properties, thereby contributing to its carcinogenic potential, including its potential impact on the transformation and progression of cancer [ 8 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

EGCG Suppresses ERK5 Activation to Reverse Tobacco Smoke-Triggered Gastric Epithelial-Mesenchymal Transition in BALB/c Mice

Lü¹,

Chen²,

Tang³

et al. 2016

Nutrients

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Tobacco smoke is an important risk factor of gastric cancer. Epithelial-mesenchymal transition is a crucial pathophysiological process in cancer development. ERK5 regulation of epithelial-mesenchymal transition may be sensitive to cell types and/or the cellular microenvironment and its role in the epithelial-mesenchymal transition process remain elusive. Epigallocatechin-3-gallate (EGCG) is a promising chemopreventive agent for several types of cancers. In the present study we investigated the regulatory role of ERK5 in tobacco smoke-induced epithelial-mesenchymal transition in the stomach of mice and the preventive effect of EGCG. Exposure of mice to tobacco smoke for 12 weeks reduced expression of epithelial markers E-cadherin, ZO-1, and CK5, while the expression of mesenchymal markers Snail-1, Vimentin, and N-cadherin were increased. Importantly, we demonstrated that ERK5 modulated tobacco smoke-mediated epithelial-mesenchymal transition in mice stomach, as evidenced by the findings that tobacco smoke elevated ERK5 activation, and that tobacco smoke-triggered epithelial-mesenchymal transition was reversed by ERK5 inhibition. Treatment of EGCG (100 mg/kg BW) effectively attenuated tobacco smoke-triggered activation of ERK5 and epithelial-mesenchymal transition alterations in mice stomach. Collectively, these data suggested that ERK5 was required for tobacco smoke-triggered gastric epithelial-mesenchymal transition and that EGCG suppressed ERK5 activation to reverse tobacco smoke-triggered gastric epithelial-mesenchymal transition in BALB/c mice. These findings provide new insights into the mechanism of tobacco smoke-associated gastric tumorigenesis and the chemoprevention of tobacco smoke-associated gastric cancer.

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“…For future work, we would like to examine molecular genetic abnormalities existing in multiple malignancies and to study their detailed roles. Environmental factors, such as smoking, eating habits and drinking, may be involved in the pathogenic process (12,13). Age may also play a role in the process of tumorigenesis, whilst most of the cases of multiple malignancies reported have happened in elderly people (14).…”

Section: Discussionmentioning

confidence: 99%