Glutathione S-transferase polymorphisms and oral cancer: A case-control study in Rio de Janeiro, Brazil

Hatagima, Ana; Costa, Emmerson C.B.; Marques, Christiane F.S.; Koifman, Rosalina Jorge; Boffetta, Paolo; Koifman, Sérgio

doi:10.1016/j.oraloncology.2007.02.001

Cited by 38 publications

(24 citation statements)

References 37 publications

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“…Corroborating our data, few studies have associated the GSTP1*B variant with UADT cancer risk (Lazarus and Park, 2000;Hashibe et al, 2003). Furthermore, our results are in accordance with those reported by other authors for the GSTP1 Ile105Val polymorphism and oral cancer risk in Brazilian populations (Leichsenring et al, 2006;Hatagima et al, 2008).…”

Section: Discussionsupporting

confidence: 93%

“…Although the GSTM1-null genotype has been shown to be a significant risk factor to different types of cancers, including lung (Lee et al, 2006), esophagus (Lu et al, 2005), and bladder (Yuan et al, 2008) cancers, this study found no association between this polymorphism and UADT cancer, in agreement with observations in other Brazilian populations (Biselli et al, 2006;Hatagima et al, 2008) and global populations (Olshan et al, 2000;Boccia et al, 2008). These results, however, do not corroborate with previous data obtained from other Brazilian populations (Drummond et al, 2004;Gattas et al, 2006).…”

Section: Discussionsupporting

confidence: 55%

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Association of the GSTT1 polymorphism in upper aerodigestive tract cancer with tobacco smoking

Silva¹,

Marques²,

Filho³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Polymorphisms in genes encoding xenobiotic-metabolizing enzymes might explain differences in the susceptibility to upper aerodigestive tract (UADT) cancers in individuals exposed to tobacco or other carcinogens. The present study aimed to evaluate the association of polymorphisms in the glutathione S-transferase (GST) candidate genes GSTM1, GSTT1, and GSTP1 with the risk of UADT cancers. GST gene polymorphisms were determined in 116 individuals with UADT cancer and 224 healthy controls using polymerase chain reaction-based methods. The GSTT1-null polymorphism was found to be a protective factor for UADT cancer [(odds ratio (OR) = 0.5, 95% confidence interval (CI) = 0.27-0.93)], although this association was not confirmed when adjusted for gender, age, smoking, alcoholism, and self-reported skin color in the multivariate logistic regression model (OR = 0.61, 95%CI = 0.29-1.28). The combined effect of GSTT1-positive genotypes with either the GSTP1 wild-type genotype (Ile/Ile) or the GSTP1 variant respectively). A significant interaction was observed among moderate smokers carrying the GSTT1-positive genotype. In this population, the significant gene-gene and gene-environment interactions of GST polymorphisms may confer a substantial risk to UADT cancers.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 55%

Association of the GSTT1 polymorphism in upper aerodigestive tract cancer with tobacco smoking

Silva¹,

Marques²,

Filho³

et al. 2014

Genet. Mol. Res.

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“…The frequency of GSTM1 null genotype ranges from 42 to 60% in Europeans, 42-54% in Asians and 16-36% in Africans; and for GSTT1 null genotype, the reported frequencies are 13-26% and 35-52% in Caucasians and Asians, respectively. 28 This study revealed that in normal controls the frequency of GSTM1 null genotype was 27.7%, the frequency of GSTT1 null genotype was 19.3% and the frequencies of GSTP1-Ile/Ile, -Ile/Val and -Val/Val genotypes were 51.8, 45.8 and 2.4%, respectively. The distribution of GSTP1 genotypes followed Hardy-Weinberg equilibrium.…”

Section: Discussionmentioning

confidence: 72%

The association of glutathione-S-transferase gene polymorphisms (GSTM1, GSTT1, GSTP1) with idiopathic male infertility

2010

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The effects of the GST genes (GSTM1, GSTT1 and GSTP1) on male factor infertility have not been well elucidated. A casecontrol study was performed to investigate the association between functionally important polymorphisms in GST genes and idiopathic male infertility. The study group consisted of 166 men suffering from idiopathic oligoasthenoteratozoospermia (OAT) and an equal number of age-matched healthy fertile male controls. Genomic DNA extracted from the peripheral blood, was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. Multivariate regression analysis showed an increase in risk to infertility in the patients with null genotype of GSTM1 (OR: 2.18; 95% CI: 1.64-3.32; P¼0.001) or GSTT1 (OR: 1.88; 95% CI:1.12-2.52; P¼0.04). Our data further showed that combination of deletion genotypes of GST (GSTM1 and GSTT1) pose an even higher risk of infertility. In addition, GSTP1 wild-type genotype in combination with GSTM1 null or GSTT1 null genotype increased probability for infertility (OR: 2.47, 95% CI: 1.46-4.17: and OR: 2.69, 95% CI: 1.39-5.32, respectively). Similarly a much higher risk for infertility was noted in the patients carrying a genotype combination of GSTM1 null, GSTT1 null and GSTP1 (Ile/Ile) (OR: 4.45; 95% CI: 1.59-12.24; P¼0.002). The variant genotypes of GSTP1 (Ile/Val and Val/Val) resulted in a significant decreased risk to infertility in the cases (OR: 0.44; 95% CI: 0.29-0.78, P¼0.004). These results support the hypothesis of increased risk of GSTM1 or GSTT1null genotypes for developing infertility, but the nondeletion GSTM1 and GSTT1genotypes emerged as protective factors.

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“…They were all case-control studies. There were two studies with overlapping subjects but reported data separately for GSTM1 71 and CYP1A1. 72 Two other studies each reported separately data for CYP1A1 Msp1 73 and exon 7.…”

Section: Selection Criteriamentioning

confidence: 99%

“…5,44,71,72,[77][78][79][80][81][82][83][84][85][86] However, two of these studies reported CYP1A1 and GSTM1 data separately for the same subjects and were counted as a single study. 71,72 Among these 13 published studies, three provided unpublished data for CYP1A1 polymorphisms for the same subjects. The GSEC database also had one study with unpublished data for GSTM1 deletion (Foulkes et al, unpublished data) and another study with unpublished data for both GSTM1 and CYP1A1 (Ruano-Ravina et al, unpublished data).…”

Section: Data Collectionmentioning

confidence: 99%

Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Varela-Lema

Taioli

Ruano-Raviña

et al. 2008

Genetics in Medicine

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The association of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers was assessed through a metaanalysis of published case-control studies and a pooled analysis of both published and unpublished case-control studies from the Genetic Susceptibility to Environmental Carcinogens database (http://www.upci.upmc.edu/research/ccps/ccontrol/ index.html). Thirty publications used in the meta-analysis included a total of 7783 subjects (3177 cases and 4606 controls); 21 datasets, 9397 subjects (3130 cases and 6267 controls) were included in the pooled analysis. The GSTM1 deletion was 2-fold more likely to occur in African American and African cases than controls (odds ratio: 1.7, 95% confidence interval: 0.9-3.3), although this was not observed among whites (odds ratio: 1.0, 95% confidence interval: 0.9-1.1). The metaanalysis and pooled analysis showed a significant association between oral and pharyngeal cancer and the CYP1A1 MspI homozygous variant (meta-OR m2/m2 : 1.9, 95% confidence interval: 1.4-2.7; Pooled OR m2m2 : 2.0, 95% confidence interval:1.3-3.1; OR m1m2 or [infi]m2m2 : 1.3, 95% confidence interval: 1.1-1.6). The association was present for the CYP1A1 (exon 7) polymorphism (OR Val/Val : 2.2, 95% confidence interval: 1.1-4.5) in ever smokers. A joint effect was observed for GSTM1 homozygous deletion and the CYP1A1 m1m2 variant on cancer risk. Our findings suggest that tobacco use and genetic factors play a significant role in oral and pharyngeal cancer. Genet Med 2008:10(6):369-384. Key Words: GSTM1, CYP1A1, oral and pharyngeal cancers, epidemiology, meta-analysis and pooled analysis Glutathione S-transferasesThe Glutathione S-transferases (GSTs) comprise a family of phase II detoxifying enzymes that catalyze a large number of reactions taking place between the cytosolic glutathione and compounds containing an electrophilic center. 1 These enzymes are involved in the elimination of xenobiotics and endogenous products of oxidative stress formed as a result of aerobic metabolism, exposure to ionizing radiation or any other process that causes cellular damage. Substrates for GSTs include acetaldehyde and several polyaromatic hydrocarbons (PAHs) found in tobacco smoke. The main steps for GST catalysis includes the formation of a complex with the cytosolic glutathione and the ionization of the sulfydryl group of this enzyme bound to glutathione to yield a highly reactive thiolate anion through hydrogen bonding with the adjacent hydroxyl

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Glutathione S-transferase polymorphisms and oral cancer: A case-control study in Rio de Janeiro, Brazil

Cited by 38 publications

References 37 publications

Association of the GSTT1 polymorphism in upper aerodigestive tract cancer with tobacco smoking

Association of the GSTT1 polymorphism in upper aerodigestive tract cancer with tobacco smoking

The association of glutathione-S-transferase gene polymorphisms (GSTM1, GSTT1, GSTP1) with idiopathic male infertility

Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

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