Interactions between Paraoxonase 1 Genetic Polymorphisms and Smoking and Their Effects on Oxidative Stress and Lung Cancer Risk in a Korean Population

Eom, Sang‐Yong; Yim, Dong‐Hyuk; Lee, Chul‐Ho; Choe, Kyu Ok; An, Jin; Lee, Kye Young; Kim, Yong‐Dae; Kim, Heon

doi:10.1371/journal.pone.0119100

Cited by 24 publications

(17 citation statements)

References 44 publications

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“…The present study showed a higher 8-OHdG expression and secretion in airways of lung cancer patients than that of noncancer controls, which was agreed with previous findings in peripheral blood and urinary [ 21 – 23 ]. Interesting, the levels of 8-OHdG in BALF were associated with the TNM stage, which indicated that oxidative DNA damage was an indicator for the development of lung cancer.…”

Section: Discussionsupporting

confidence: 94%

Smoking-promoted oxidative DNA damage response is highly correlated to lung carcinogenesis

Cao

Lai

et al. 2016

Oncotarget

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Oxidative stress induced by tobacco smoking is one of the main causes of DNA damage and is known to be involved in various cancers. Smoking is the leading cause of lung cancer, while the role of cigarette smoke-induced oxidative DNA damage response during lung carcinogenesis is largely unknown. In this study, we investigated oxidative DNA damage response levels in smoking and nonsmoking patients with lung cancer, and evaluated the potential diagnostic value of 8-OHdG for lung cancer. We observed a higher level of 8-OHdG expression and secretion in airways of lung cancer patients than that of noncancer controls. 8-OHdG expression was associated with the TNM stages. Additionally, cigarette smoke-induced oxidative DNA damage response was observed in bronchial epithelial cells in vitro and in vivo. A statistical significance correlation was found between the levels of 8-OHdG and smoking index. With a cut-off value of 2.86 ng/ml, 8-OHdG showed a sensitivity and specificity of 70.0% and 73.7%, respectively, to identify a patient with lung cancer. These findings not only underscore the importance of smoking in oxidative DNA damage response of lung cancer patients, but also suggest 8-OHdG as a potential diagnostic biomarker for lung cancer.

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Section: Discussionsupporting

confidence: 94%

Smoking-promoted oxidative DNA damage response is highly correlated to lung carcinogenesis

Cao

Lai

et al. 2016

Oncotarget

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“…43 Moreover, a strong linkage disequilibrium between the CYP3A4 rs2242480 and CYP3A5 rs776746 polymorphism was reported by several studies. 16,44 There are more and more studies considering genegene or gene-environment interaction in relationship with various diseases and drugs, such as breast cancer, 45 lung cancer, 35,46 warfarin, 47 and coumarins. [38][39][40] Unlike traditional pharmacogenetics analysis focused only on a single SNP, gene-gene and gene-environment interactions take genetic and environmental context into account, which is more powered in complex diseases and drug responses.…”

Section: Discussionmentioning

confidence: 99%

Incorporation of Gene‐Environment Interaction Terms Improved the Predictive Accuracy of Tacrolimus Stable Dose Algorithms in Chinese Adult Renal Transplant Recipients

Tang

Zhang

et al. 2019

The Journal of Clinical Pharma

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The narrow therapeutic window of tacrolimus necessitates daily monitoring and predictive algorithms based on genetic and nongenetic factors. In this study, we constructed predictive algorithms for tacrolimus stable dose in a retrospective cohort of 1045 Chinese renal transplant recipients. All patients were genotyped for CYP3A4 20230T>C (rs2242480), CYP3A4 T>C (rs4646437), CYP3A5*3 6898A>G (rs776746), ABCB1 129T>C (rs3213619); ABCB1 c.1236C>T (rs01128503), ABCB1 c.2677G>T/A (rs2032582) and ABCB1 c.3435C>T (rs1045642) polymorphisms, and the effects of gene‐gene and gene‐environment interactions on the predictive accuracy of algorithm were evaluated. In wild‐type CYP3A4 rs2242480 (TT) carriers, patients who took calcium channel blockers had lower tacrolimus stable doses than those without the concomitant medications (P < 1 × 10−4). In contrast, there was no significant difference in mutant type patients. Similarly, the tacrolimus stable doses in wild‐type CYP3A5 rs776746 carriers who had hypertension were higher than those without hypertension (P = 4.10 × 10−3). More importantly, dose‐predictive algorithms with interaction terms showed higher accuracy and better performance than those without interaction terms. Our finding suggested that wild‐type CYP3A4 rs2242480 (TT) carriers should be more cautious to take tacrolimus when they are coadministrated with calcium channel blockers, and CYP3A5 rs776746 (AA) carriers may need higher tacrolimus dosage when they are in combination with hypertension.

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“…Only CYP1A2 was associated with the genetic polymorphisms present in gastric cancer. The effect of AFB 1 on gastric carcinogenesis may not be modulated by genetic polymorphisms of AFB 1 metabolic enzymes [111].…”

Section: Epigeneticsmentioning

confidence: 98%

Metabolic Changes of Aflatoxin B1 to become an Active Carcinogen and the Control of this Toxin

Carvajal-Moreno¹

2015

Immunome Res

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Although aflatoxins are unavoidable toxins of food, many methods are available to control them, ranging from natural detoxifying methods to more sophisticated ones. The present review englobes the main characteristics of Aflatoxins as mutagens and carcinogens for humans, their physicochemical properties, the producing fungi, susceptible crops, effects and metabolism. In the metabolism of Aflatoxins the role of cytochromes and isoenzymes, epigenetics, glutathione-S-transferase enzymes, oncogenes and the role of aflatoxins as mutagens of the tumor suppressor gene p53, and the Wnt signaling pathway are briefly explained, as well as these toxins as biomarkers.The last section includes the Aflatoxin control methods, from the protection of the crop from the Aspergillus fungi, the biocontrol solution, the AFB1-DNA adduct control with the natural repair rates of adduct removal, induction to resistance to AFB1, the detoxification enzymes, recombinant yeasts, pre-exposure to Aflatoxin M1, the inhibition of AFB1 lesions by different compounds, chemoprevention and protective chemical compounds, cruciferous vegetables, dietary dithiolethiones, glucoraphanin, indol-3-carbinol, oltipraz, phenols (butylated hydroxytoluene and ellagic acid), indomethacin, selenium, natural nutrients, coumarin chemoprevention, cafestol and kahweol, terpenes and monoterpenes, grapefruit juice, vitamins, traditional Chinese medical plants (Oldenlandia diffusa and Scutellaria barbata), chlorophyllin, probiotic bacteria and additives as aluminosilicates and glucomannans are described here. Finally, the aflatoxin international legislation was briefly described.

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Interactions between Paraoxonase 1 Genetic Polymorphisms and Smoking and Their Effects on Oxidative Stress and Lung Cancer Risk in a Korean Population

Cited by 24 publications

References 44 publications

Smoking-promoted oxidative DNA damage response is highly correlated to lung carcinogenesis

Smoking-promoted oxidative DNA damage response is highly correlated to lung carcinogenesis

Incorporation of Gene‐Environment Interaction Terms Improved the Predictive Accuracy of Tacrolimus Stable Dose Algorithms in Chinese Adult Renal Transplant Recipients

Metabolic Changes of Aflatoxin B1 to become an Active Carcinogen and the Control of this Toxin

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