Microsomal epoxide hydrolase and glutathione S-transferase polymorphisms in relation to laryngeal carcinoma risk

To‐Figueras, Jordi; Gené, M.; Gómez‐Catalán, Jesús; Piqué, Ester; Borrego, N.; Caballero, Miguel; Cruellas, Francesc; Raya, Anna; Dicenta, Manuel; Corbella, Jacint Corbella i

doi:10.1016/s0304-3835(02)00406-8

Cited by 57 publications

(40 citation statements)

References 33 publications

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“…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: 82%

“…[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: 82%

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 by several groups provided invaluable data on genotypic polymorphism in various cancers including lung cancer, and indicated that a detection rate of 340 TAC allele (Tyr113) in exon 3 ranged from 0.63 to 0.77, and that of 418 CAT (His139) in exon 4 ranged from 0.77 to 0.94 (10)(11)(12)(13)(14)(15) (Tables I and II). A parallel study on normal population would help to determine whether the imbalanced allelic expression of mEH observed in NSCLC patients is disease-related.…”

Section: Discussionmentioning

confidence: 99%

“…When 295-and 62-bp fragments appeared, the patient had homozygous allele of His139. When 174-, 121-and 62-bp bands appeared, the patient was identified as homozygous Arg139 allele, and when all four DNA fragments appeared, the patient was heterozygous with His139/Arg139 (1,(8)(9)(10)(11)(12)(13)(14)(15).…”

Section: Methodsmentioning

confidence: 99%

“…The enzyme with Tyr113 (fast type) has 50% higher activity than that with His113 (slow type), whereas mEH with His139 (slow type) has only 25% activity of that with Arg139 (fast type) (8). Previous studies indicate that the mEH enzyme with Tyr113 (fast type) is closely associated with the increased risk of lung, breast, laryngeal and colon cancers (10)(11)(12)(13)(14)(15). In particular, when patients with higher mEH activity (fast type) were exposed frequently to tobacco smoking, cancer risk increased significantly (16,17).…”

Section: Introductionmentioning

confidence: 99%

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Genetic polymorphism and gene expression of microsomal epoxide hydrolase in non-small cell lung cancer

Lin

Huang²,

Fan³

et al. 2007

Oncol Rep

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Abstract. Genetic polymorphisms of microsomal epoxide hydrolase (mEH) have been associated with increased risk of lung cancer. However, expression of mEH and its clinical significance in non-small cell lung cancer (NSCLC) have not been investigated. In this study we investigated the expression and genetic polymorphism of mEH in non-small cell lung cancer (NSCLC) patients. Genetic polymorphism was determined by restriction fragment length polymorphism of polymerase chain reaction (PCR) products. CGT/ 418 CGT in exon 4. Of the 72 NSCLC biopsies analyzed, mEH was expressed in 60 (83%) surgical specimens, and the major allelic expression pattern was fast type (Tyr113) in exon 3 (90.3%) and slow type (His139) in exon 4 (100%). Immunohistochemical staining showed that mEH was expressed in 326 of 423 (77.0%) tumor (lung tissue) specimens and in 48 of 93 (51.6%) metastatic lymph nodes. A significant difference in patient survival was found when mEH expression and adriamycin-containing chemotherapy were used to group patients (p=0.0167). In conclusion, with the combination of fast type (Tyr113) and slow type (His139), the mEH enzyme expressed in most NSCLC patients may have intermediate activity. Our findings indicate that with respect to cancer risk and disease progression, the expression level of mEH is as important as genetic polymorphism. In addition, mEH expression in NSCLC could be involved in drug resistance and prognosis of patients.

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Use of biomarkers to elucidate genetic susceptibility to cancer

Salama

2005

Environ and Mol Mutagen

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Genetic variations have generally been accepted to be the major mechanism for the differences observed in susceptibility to cancer. However, extensive investigations on genotype-disease associations have not produced consistent results. The inconsistency may be caused by many factors, such as improper study design, insufficient sample size, complexity of the traits under investigation, heterogeneity of the study subjects, incorrect assumptions about the underlying genetic architecture, misclassification of the disease, improper selection of potential alleles, and overinterpretation of the data. Besides these "traditional" factors, a recent problem is that the function of many variant genotypes is unknown, especially with regard to polymorphic DNA repair genes. Therefore, in addition to the genotype-disease relationship, it may be prudent to step back and investigate the fundamental role of genetic variation in the development of cancer. The latter studies may focus on understanding the genotype-exposure interactions and evaluating genotype-health risk associations. This review will emphasize the use of relevant biomarkers and polymorphic DNA repair genes for investigations. These data will be useful for a better understanding of the complexity of disease causation and development, developing new models for human disease, and identifying pathways for prevention of cancer.

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Microsomal epoxide hydrolase and glutathione S-transferase polymorphisms in relation to laryngeal carcinoma risk

Cited by 57 publications

References 33 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

Genetic polymorphism and gene expression of microsomal epoxide hydrolase in non-small cell lung cancer

Use of biomarkers to elucidate genetic susceptibility to cancer

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