Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms and lung cancer risk among Northwestern Mediterraneans

To‐Figueras, Jordi; Gené, M.; Gómez‐Catalán, Jesús; Galan, MaCarmen; Fuentes, Mariana Terán; Ramón, Josep; Rodamilans, M.; Huguet, E.; Corbella, Jacint Corbella i

doi:10.1093/carcin/18.8.1529

Cited by 101 publications

(40 citation statements)

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“…Results have not supported an association with lung cancer risk (To-Figueras et al, 1997;Malats et al, 2000;Stucker et al, 2002;Ruano-Ravina et al, 2003;Wang et al, 2003b). In bladder cancer, the association is not consistent (Abdel-Rahman et al, 1998).…”

Section: Carcinogen Metabolismmentioning

confidence: 96%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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Although cigarette smoking is the dominant risk factor for several epithelial cancers, only a small fraction of individuals with tobacco exposure develop cancer. The underlying hypothesis is that genetic factors may render certain smokers more susceptible to cancer than others. Genetic alterations in critical regulatory pathways may predispose cells to carcinogenesis. These pathways include regulation of xenobiotic metabolism; control of genomic stability, including DNA repair mechanisms, cell-cycle checkpoints, apoptosis and telomere length; and control of microenvironmental factors, such as matrix metalloproteinases, inflammation and growth factors. In addition, epigenetic events, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis. In this review, we will summarize recent advances in genetic susceptibility to tobacco-related cancer. Emphasizing on risk assessment, we will describe how genetic variations in the above-mentioned genetic pathways modify the tobacco-related cancer risk. In addition, we will discuss how genetic variations may assist in predicting clinical outcome, such as the natural history of cancer and treatment response. The measurements of genetic susceptibility by both genotypic and phenotypic assays are covered in the text. Finally, we present a number of current concerns that need to be addressed as the exciting field of molecular cancer epidemiology advances rapidly.

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Section: Carcinogen Metabolismmentioning

confidence: 96%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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“…The GSTM1 polymorphism, which is the deletion of the GSTM1 gene leading to the absence of the enzyme, has been reported to be a moderate risk factor for the development of lung cancer (Alexandrie et al, 1994). The GSTT1 polymorphism is also caused by a deletion that results in the total lack of gene product (Alexandrie et al, 2000), deficiency in this enzyme having been correlated with an increased risk of lung cancer (To-Figueras et al, 1997). The GSTP1 polymorphisms GSTP1 (Ile105 Val) and GSTP1 (Ala114 Val) also lead to a decrease in the activity of the corresponding enzyme (Watson et al, 1998), and it has recently been shown that the GSTP1 polymorphism is associated with an increase risk of lung carcinoma (Wang et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Cytochrome P450 (CYP) and glutathione S-transferases (GST) polymorphisms (CYP1A1, CYP1B1, GSTM1, GSTP1 and GSTT1) and urinary levels of 1-hydroxypyrene in Turkish coke oven workers

et al. 2007

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Genetic polymorphisms of xenobiotic metabolizing enzymes have been associated with cancer risk. We evaluated the influences of genetic polymorphisms of polycyclic aromatic hydrocarbon (PAH) metabolizing enzymes on urinary 1-hydroxypyrene (1-OHP) excretion in Turkish coke oven workers. Urinary 1-OHP was analyzed by HPLC after enzymatic hydrolysis. Lymphocyte DNA was used for PCR-based genotyping of cytochrome P450 (CYP) polymorphisms (CYP1A1 and CYP1B1) and glutathione S-transferases (GST) polymorphisms (GSTM1, GSTT1 and GSTP1). The mean urinary 1-OHP levels of coke oven workers were significantly higher than that of controls. No significant difference was detected in the mean urinary 1-OHP levels of smokers and non-smokers either for coke oven workers or controls. Genetic polymorphisms of the CYPs and GSTs studied had no significant influence on 1-OHP excretion in coke oven workers, but in the control group the urinary 1-OHP levels of individuals carrying the GSTT1-genotype were significantly higher than those of individuals carrying GSTT1+ genotype. The duration of occupational exposure and metabolic genotype for GSTT1 were the significant predictors of urinary 1-OHP levels. The control individuals carrying combined GSTM1-/GSTT1-genotypes also had significantly higher levels of urinary 1-OHP than those of individuals carrying GSTM1+/GSTTI+, GSTM1-/GSTT1+, and GSTM1+/GSTT1-genotypes. These results indicate that urinary 1-OHP is a sensitive indicator of recent human exposure to PAHs and that genetic polymorphism of GSTT1 may also to some extent reflect the interindividual variation in susceptibility to PAHs only at low PAH exposure.

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“…[13], [18] Several Caucasian studies were previously conducted to assess the role of GSTT1 in lung cancer susceptibility with the case-control approach. [10], [11], [19][20][21][22] No significant associations of GSTT1 with lung cancer risk could be established, and two of the studies found that the GSTT1 null genotype did not elevate the risk with either lung adenocancer or squamous cell carcinoma. [19], [20] Another study in Chinese found that the GSTT1 genotype was not related to lung cancer.…”

Section: Discussionmentioning

confidence: 99%

The frequency of GSTT1 null genotype in Turkish population and lung cancer risk

Demir¹,

Altın²,

Demir³

et al. 2005

Indian J Hum Genet

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BACKGROUND:Previous studies have suggested that Glutathione S-transferase (GST) genotypes may play a role in determining susceptibility to lung cancer, though the data are often conflicting. In different ethnic groups variations in null allele frequency has been observed. AIMS: We aimed to evaluate whether genetic polymorphisms of Glutathione S-transferase theta (GSTT1) influence individual susceptibility to lung cancer in Turkish population. We tried to clarify the frequencies of GSTM1 gene polymorphisms in a Turkish population. METHODS: DNA samples, extracted from the whole blood were amplified using polymerase chain reaction (PCR) method in all of the 68 cases, composed of 31 previously diagnosed lung cancer and 37 healthy controls. RESULTS: The prevalence of GSTT1 null genotype in the lung cancer patients was 29%, compared to 11% in control group. GSTT1 null genotype was found to be higher in cancer group compared to the control group, although it was not statistically significant (OR = 3.37, 95% CI = 0.92-12.32, P = 0.06). There was also no significant relation in GSTT1 genotypes among histopathology types of lung cancers. The frequency of GSTT1 was found to be 25.4% (n = 952) when the studies of Turkish population were reviewed. CONCLUSION: It can be concluded that carrying the GSTT1 null genotype may be accepted as a weak risk factor for the susceptibility to lung cancer.Key words: Genetic polymorphism; GSTT1 and molecular epidemiology; lung cancer. Lung cancer is the most common malignancy and the leading cause of cancer death in men world wide and also the second most lethal cancer in women after breast cancer.[1], [2] Active and passive smoking, various occupational exposures, and carcinogens in heavily

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Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms and lung cancer risk among Northwestern Mediterraneans

Cited by 101 publications

References 5 publications

Genetic susceptibility to tobacco-related cancer

Genetic susceptibility to tobacco-related cancer

Cytochrome P450 (CYP) and glutathione S-transferases (GST) polymorphisms (CYP1A1, CYP1B1, GSTM1, GSTP1 and GSTT1) and urinary levels of 1-hydroxypyrene in Turkish coke oven workers

The frequency of GSTT1 null genotype in Turkish population and lung cancer risk

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