Investigation of genetic polymorphisms and smoking in a bladder cancer case–control study in Argentina

Moore, Lee E.; Wiencke, John K.; Bates, Michael; Zheng, Shichun; Rey, Omar A.; Smith, Allan H.

doi:10.1016/j.canlet.2004.04.011

Cited by 72 publications

(57 citation statements)

References 35 publications

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“…These include scraping with a wood spatula (31,34,48,51,52,60,62,91,92), wood tongue depressor (12,32,43,45,56), cotton swab (42), short-bristle cytobrush (28,29,33,40,44,57,95,96), and toothbrush (95,96).…”

Section: Resultsmentioning

confidence: 99%

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Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Proia

Paszkiewicz

Nasca³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

144

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Reported herein are the results of a structured literature review that was undertaken to (a) determine if human buccal (mouth) cell changes are associated with smoking and smokeless (''chewing'') tobacco, (b) tabulate different buccal cell alterations that have been reported, (c) delineate buccal cell assays that have been used successfully, (d) determine whether buccal cell changes correlate with oral cancer as defined in clinicopathologic investigations, and (e) assess the feasibility of developing a high-throughput buccal cell assay for screening smokers for the early detection of oral cancer. The results of the studies reported herein have established that diverse buccal cell changes are associated with smoking and smokeless tobacco. This review documents also that buccal cells have been collected in a noninvasive manner, and repetitively for serial studies, from different sites of the mouth (e.g., cheek, gum, and tongue) and from normal tissue, preneoplastic lesions (leukoplakia), and malignant tumors. Tobacco-associated genetic mutations and nongenetic changes have been reported; a partial listing includes (a) micronuclei, (b) bacterial adherence, (c) genetic mutations, (d) DNA polymorphisms, (d) carcinogen-DNA adducts, and (e) chromosomal abnormalities. Clinical studies have correlated buccal cell changes with malignant tumors, and some oral oncologists have reported that the buccal cell changes are practical biomarkers. Summarily, the literature has established that buccal cells are useful not only for characterizing the molecular mechanisms underlying tobacco-associated oral cancers but also as exfoliative cells that express diverse changes that offer promise as candidate biomarkers for the early detection of oral cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(6):1061 -77)

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Section: Resultsmentioning

confidence: 99%

“…The tests for assessing buccal cell changes associated with smoking included procedures that employed PCR (n = 10 articles; refs. 25,26,30,32,35,36,40,41,45,47) and DNA adduct technology (n = 9; refs. 38, 39, 46, 48, 49, 54, 57-59; Table 1).…”

Section: Gudakhu Yesmentioning

confidence: 99%

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Proia

Paszkiewicz

Nasca³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

144

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“…We identified nine studies examining the effect of the NQO1 Pro187Ser polymorphism on the risk of bladder cancer (46)(47)(48)(49)(50)(51)(52)(53)(54); one study (51) was excluded due to the lack of genotype information. The remaining eight studies included a total of 1,410 cases and 1,485 controls.…”

Section: Resultsmentioning

confidence: 99%

NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Pro187Ser Polymorphism and the Risk of Lung, Bladder, and Colorectal Cancers: a Meta-analysis

Chao

Zhang

Berthiller³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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NAD(P)H:quinone oxidoreductase 1 (NQO1) is a cytosolic enzyme that catalyzes the two-electron reduction of quinoid compounds into hydroquinones, their less toxic form. A sequence variant at position 609 (C ! T) in the NQO1 gene encodes an enzyme with reduced quinone reductase activity in vitro and thus was hypothesized to affect cancer susceptibility. We conducted meta-analyses focusing on three cancer sites (lung, bladder, and colorectum) to summarize the findings from the current literature and to explore sources of heterogeneity. Results: There is no clear association between the NQO1 Pro187Ser polymorphism and lung cancer risk in the three ethnic groups examined: odds ratio (OR White ) C/T + T/T versus C/C = 1.04 [95% confidence interval (95% CI), 0.96-1.13], OR Asian = 0.99 (95% CI, 0.72-1.34), and OR Blacks = 0.95 (95% CI, 0.66-1.36). However, a modestly increased risk was suggested for the variant homozygotes in whites (OR T/T versus C/C, 1.19; 95% CI, 0.94-1.50). Analysis excluding one outlier study suggested the variant allele may be associated with reduced lung cancer risk in Asians. Meta-analyses for bladder and colorectal cancer suggested a statistically significant association with the variant genotypes in whites. In stratified analyses, the NQO1 Pro187Ser variant genotypes were associated with slightly increased lung cancer risk in white ever smokers but not in white never smokers and were mainly associated with a reduced risk of lung adenocarcinoma but not squamous cell carcinoma in Asians. Conclusions: Results from our meta-analyses suggest that the variant NQO1 Pro187Ser genotype may affect individual susceptibility to lung, bladder, and colorectal cancer. Such effects of the NQO1 polymorphism seem to be modified by ethnicity and smoking status.

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“…After further retrieved, 12 articles were excluded because of the following reasons: three were for review or meta-analysis articles (Gonzalez, 1997;Chao et al, 2006;Ersoy Tunali et al, 2011); one did not focus on the NQO1 rs1800566 polymorphism but on NQO2 (exon 3, T14055C) polymorphism (Wen et al, 2009); two were for the correlation between the NQO1 rs1800566 polymorphism and NQO1 activity (Basu et al, 2004;Jamieson et al, 2007); two were for the correlation between the NQO1 rs1800566 polymorphism and p53 mutations (Martone et al, 2000;Ryk et al, 2006); one was for the correlation between the NQO1 rs1800566 polymorphism and clinical course of bladder cancer (Sanyal et al, 2007); Three studies did not report gene frequencies (Vineis et al, 2007;Dhaini et al, 2012;Ersoy Tunali et al, 2012). Therefore, 12 studies (Schulz et al, 1997;Choi et al, 2003;Park et al, 2003;Hung et al, 2004;Moore et al, 2004;Sanyal et al, 2004;Broberg et al, 2005;Terry et al, 2005;Figueroa et al, 2008;Wang et al, 2008;Paonessa et al, 2009;Pandith et al, 2011) were included in our meta-analysis. The detailed characteristics of the included studies were shown in Table 2.…”

Section: Characteristics Of All Included Studiesmentioning

confidence: 99%

The NQO1 rs1800566 Polymorphism and Risk of Bladder Cancer: Evidence from 6,169 Subjects

Guo¹,

Feng²

2012

Asian Pacific Journal of Cancer Prevention

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Investigation of genetic polymorphisms and smoking in a bladder cancer case–control study in Argentina

Cited by 72 publications

References 35 publications

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

NAD(P)H:Quinone Oxidoreductase 1 (NQO1) Pro187Ser Polymorphism and the Risk of Lung, Bladder, and Colorectal Cancers: a Meta-analysis

The NQO1 rs1800566 Polymorphism and Risk of Bladder Cancer: Evidence from 6,169 Subjects

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