GSTM1 polymorphism and oral squamous cell carcinoma

Drummond, Sérgio Neves; Marco, Luiz; Noronha, Júlio Carlos; Gomez, Ricardo Santiago

doi:10.1016/s1368-8375(03)00132-5

Cited by 41 publications

(40 citation statements)

References 18 publications

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“…Our study showed similar frequencies for these genotypes (24.4 and 17.8% for GSTT1 [-] in patients and controls, and 44.4 and 48.9% for GSTM1 [-] in patients and controls). Higher GSTT1 [-] and GSTM1 [-] polymorphism frequencies were observed by Drummond et al 21,22 in Brazilian smokers with oral cavity squamous cell carcinoma (81.8% for GSTT1 [-] and 70.5% for GSTM1 [-] 15,20,22,44 which was not seen in other studies. 5,16,37,39,41,43,46 The combination of these higher risk and null genotypes has also been observed in this type of carcinoma.…”

Section: Discussionmentioning

confidence: 56%

“…[13][14][15][16][17][18][19][20][21][22] Two genes in particular -GSTT1 and GSTM1 -that code phase II enzymes belonging to the glutathione S-transferases (GSTs) family seem relevant for susceptibility to head and neck squamous cell carcinoma; they detoxify carcinogenic tobacco smoke reactive metabolites. [11][12]13,15,18,20,23 The GSTM1 gene is polymorphic in humans, including a null-activity allele (GSTM1-) due to a major genic deletion, and two functional alleles (GSTM1A and GSTM1B).…”

Section: Introductionmentioning

confidence: 99%

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Polimorfismos GSTT1 e GSTM1 em indivíduos tabagistas com carcinoma espinocelular de cabeça e pescoço

Biselli

Leal

Ruiz

et al. 2006

Rev. Bras. Otorrinolaringol.

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Gene variability related to carcinogen activation and detoxification may interfere with susceptibility to head and neck cancer. Aim: To investigate the relation between GSTT1 and GSTM1 null polymorphisms and the risk of head and neck squamous cell carcinoma in cigarette smokers. Material and Method: A case-control study conducted at the Sao Jose do Rio Preto Medical School, Brazil. GSTM1 and GSTT1 null genotype frequencies were evaluated by multiplex PCR in 45 cigarette smokers with head and neck squamous cell carcinomas and 45 cigarette smokers without this disease. Results: The oral cavity was the most prevalent tumor site for squamous cell carcinoma. The GSTT1 null genotype was found in 33.3% of the Experimental Group and 23.3% of the Control Group (p= 0.311). Experimental and Control Groups had GSTM1 null genotype frequencies of 35% and 48.3% (p=0.582). No association between alcohol consumption and GSTT1 and GSTMI null genotypes was found in these groups (p-values>0.05). There were more men, and alcohol consumption was prevalent in both groups. Conclusion: In this study we were unable to show a correlation between GSTM1 and GSTT1 genotypes and the development of head and neck squamous cell carcinomas in cigarette smokers.

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Section: Discussionmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Polimorfismos GSTT1 e GSTM1 em indivíduos tabagistas com carcinoma espinocelular de cabeça e pescoço

Biselli

Leal

Ruiz

et al. 2006

Rev. Bras. Otorrinolaringol.

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“…Previous studies as well as the present study failed to observe any risk of 2/2 genotype at codon 72 of p53 for the oral cancer and HNSCC. [26][27][28][29][30][31][32][33][34] Thus, it appears that individuals with specific p53 genotypes are more susceptible to the development of tobacco-assisted oral leukoplakia, indicating a possible role of 2/2 variant of p53 codon 72 in early stages of oral cancer development. We speculate that processing of the signals generated from the tobacco-associated DNA damage is differentially regulated depending on both specific p53 variant present and the developmental stage of the incipient tumor.…”

Section: Discussionmentioning

confidence: 99%

“…So far, only a few studies have reported a lack of association of the p53 codon 72 2/2 genotype with susceptibility to head and neck squamous cell carcinoma, [26][27][28][29][30][31][32][33][34] but significant difference in haplotype frequency between head and neck cancer patients and controls has been observed. 32 To date, there is no report on association of a particular p53 genotype and/or haplotype in tobaccoassociated leukoplakia.…”

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confidence: 99%

Risk assessment of p53 genotypes and haplotypes in tobacco‐associated leukoplakia and oral cancer patients from eastern india

Mitra

Sikdar

Misra

et al. 2005

Intl Journal of Cancer

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The role of 3 p53 polymorphisms (16 bp duplication at intron 3, codon 72 Arg/Pro and intron 6 NciI RFLP at np 13494) as potential markers for indicating cancer risk remains inconclusive. In our case-control study consisting of 197 leukoplakia and 310 oral squamous cell carcinoma (SCC) patients and 348 controls, genotype frequencies at these 3 p53 loci were determined by PCR-RFLP method and analyzed by multiple logistic regression to determine the risks of the diseases. The 2/2 genotype at codon 72 of p53 was at risk for developing leukoplakia (OR 5 1.6, 95% CI 1.1-2.3), whereas the combination of 1/2 and 2/2 genotypes at intron 3 and 1/1 and 1/2 genotypes at intron 6 conferred a protective effect against leukoplakia and oral SCC development, respectively (OR 5 0.5, 95% CI 0.4-0.8 and OR 5 0.6, 95% CI 0.5-0.9, respectively). When subjects were stratified according to specific tobacco habit, the risk/protection estimates improved significantly in some cases. Specifically, the exclusive smokers with p53 codon 72 2/2 genotype showed a higher risk of developing leukoplakia (OR 5 2.7, 95% CI 1.2-6.3). Furthermore, a particular p53 haplotype 1-2-2 was at risk for both tobacco-associated leukoplakia and oral SCC (OR 5 1.5, 95% CI 1.1-1.9 and OR 5 1.3, 95% CI 1.1-1.7, respectively). Our results show that both specific p53 genotype and haplotype can indicate risk of tobacco-associated leukoplakia, but risk of development of tobacco-associated oral SCC can be predicted by specific p53 haplotype only. ' 2005 Wiley-Liss, Inc.

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“…8 In addition, many studies have demonstrated that susceptibility to oral cancer is associated with phase I and phase II metabolic enzymes. [9][10][11] It has also been suggested that the detection of genetic changes such as DNA aneuploidy and loss of heterozygosity could improve the possibilities for predicting malignant development from precursor lesions. 12 However, there are no reliable biomarkers to predict which oral leukoplakias will be quiescent or will rapidly become invasive squamous cell carcinoma.…”

Section: Introductionmentioning

confidence: 99%

Molecular alterations in the tumor suppressor gene WWOX in oral leukoplakias

et al. 2008

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SummaryOral leukoplakia is the most prevalent and potentially malignant disorder of the oral mucosa. Previous studies have demonstrated that molecular changes of the WWOX gene (WW-domain containing oxidoreductase), a candidate tumor suppressor gene located at 16q23.3-24.1 that spans FRA16D, the second most common fragile site, are present in several malignant neoplasias, including oral squamous cell carcinoma. In this report, the role of the WWOX gene was investigated in 23 cases of oral leukoplakias. Using nested RT-PCR and immunohistochemistry, altered mRNA transcription and/or reduced Wwox protein expression was observed in 35% of the lesions when compared with normal mucosa. The majority of lesions (4/6) with altered transcripts had a reduction in the expression of Wwox protein. Although normal WWOX expression was found in some lesions with dysplasia, all lesions with WWOX mRNA and/or protein expression showed histological evidence of dysplasia and none of the cases without dysplasia presented this alteration. These results show that the WWOX gene alteration is an early genetic alteration and may contribute to oral carcinogenesis.

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GSTM1 polymorphism and oral squamous cell carcinoma

Cited by 41 publications

References 18 publications

Polimorfismos GSTT1 e GSTM1 em indivíduos tabagistas com carcinoma espinocelular de cabeça e pescoço

Polimorfismos GSTT1 e GSTM1 em indivíduos tabagistas com carcinoma espinocelular de cabeça e pescoço

Risk assessment of p53 genotypes and haplotypes in tobacco‐associated leukoplakia and oral cancer patients from eastern india

Molecular alterations in the tumor suppressor gene WWOX in oral leukoplakias

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