Background The association of the three Glutathione S-transferases (GSTs) polymorphisms (GSTM1, GSTT1 and GSTP1) genotypes with their individual susceptibilities to renal cell carcinoma (RCC) has not been well established. We performed a quantitative meta-analysis to assess the possible associations between the GSTM1, GSTT1 and GSTP1 genotypes and their individual susceptibilities to renal cell carcinoma. Methods We systematically searched the PubMed, CNKI and Embase databases to identify the relevant studies. Finally, 11 eligible studies were selected. The pooled odds ratios (ORs) with their 95% confidence intervals (CIs) were used to assess the association between the GSTs polymorphisms and the risk of RCC. Multiple subgroup analyses and quality assessment of the included studies were performed based on the available information. Results None of the GSTs polymorphisms had a significant association with the RCC risk. Similar results were found in the subgroup analyses, except for the GSTs polymorphisms in the situations described below. The GSTM1 and GSTT1 active genotypes in subjects exposed to pesticides (GSTM1: OR = 3.44; 95% CI, 2.04–5.80; GSTT1: OR = 2.84; 95% CI, 1.75–4.60), most of the GSTs genotypes in Asian populations (GSTT1: OR = 2.39, 95% CI = 1.63–3.51; GSTP1: Dominant model: OR = 1.50, 95% CI = 1.14–1.99; Additive model: OR = 1.39, 95% CI = 1.12–1.73; AG vs. AA: OR = 1.47, 95% CI = 1.10–1.97; GG vs. AA: OR = 1.82, 95% CI = 1.07–3.09) and the dual null genotype of GSTT1-GSTP1 (OR = 2.84, 95% CI = 1.75–4.60) showed positive associations with the RCC risk. Conclusion Our present study provides evidence that the GSTM1, GSTT1 and GSTP1 polymorphisms are not associated with the development of RCC. However, more case-control studies are needed for further confirmation.
References
[1]
Ferlay J, Shin HR, Bray F, Forman D, Mathers C, et al. (2010) Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 127: 2893–2917.
[2]
Landis SH, Murray T, Bolden S, Wingo PA (2008) Cancer statistics, 1999. CA: A cancer J Clin 49: 8–31.
[3]
Curado MP, Edwards B, Shin HR, Storm H, Ferlay J, et al. (2008) Cancer incidence in five continents.Katner HP, Baynham SA (1999) Increasing incidence of renal cell cancer. JAMA 282: 2119–2121.
[4]
Katner HP, Baynham SA (1999) Increasing incidence of renal cell cancer. JAMA 282: 2119–2121.
[5]
Chow WH, Devesa SS, Warren JL, Fraumeni Jr JF (1999) Rising incidence of renal cell cancer in the United States. JAMA 281: 1628–1631.
[6]
Vineis P, Alavanja M, Buffler P, Fontham E, Franceschi S, et al. (2004) Tobacco and cancer: recent epidemiological evidence. J Natl Cancer Inst 96: 99–106.
[7]
Adams KF, Leitzmann MF, Albanes D, Kipnis V, Moore SC, et al. (2008) Body size and renal cell cancer incidence in a large US cohort study. American journal of epidemiology 168: 268–277.
[8]
Facchini F, Ida Chen Y, Reaven GM (1994) Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity. Diabetes care 17: 115–119.
[9]
Hayes JD, Pulford DJ (1995) The Glut athione S-Transferase Supergene Family: Regulation of GST and the Contribution of the lsoenzymes to Cancer Chemoprotection and Drug Resistance Part II. Crit Rev Biochem Mol Biol. 30: 521–600.
[10]
Ketterer B (1988) Protective role of glutathione and glutathione transferases in mutagenesis and carcinogenesis. Mutat Res 202: 343–361.
[11]
Seidegard J, Pero RW, Miller DG, Beattie EJ (1986) A glutathione transferase in human leukocytes as a marker for the susceptibility to lung cancer. Carcinogenesis 7: 751–753.
[12]
Ye Z, Song H (2005) Glutathione s-transferase polymorphisms (GSTM1, TSTP1 and GSTT1) and the risk of acute leukaemia: A systematic review and meta-analysis. Eur J Cancer 41: 980–989.
[13]
Sergentanis TN, Economopoulos KP (2010) GSTT1 and GSTP1 polymorphisms and breast cancer risk: a meta-analysis. Breast Cancer Res Treat 121: 195–202.
[14]
Shi X, Zhou S, Wang Z, Zhou Z (2008) CYP1A1 and GSTM1 polymorphisms and lung cancer risk in Chinese populations: a meta-analysis. Lung Cancer 59: 155–163.
[15]
Sui Y, Han W, Yang Z, Jiang M, Li J (2011) Association of glutathione S-transferase M1 and T1 null polymorphisms with the development of cervical lesions: a meta-analysis. Eur J Obstet Gynecol Reprod Biol 159: 443–448.
[16]
Pearson W, Vorachek W, Xu S, Berger R, Hart I, et al. (1993) Identification of class-mu glutathione transferase genes GSTM1-GSTM5 on human chromosome 1p13. Am J Hum genet 53: 220.
[17]
Webb G, Vaska V, Coggan M, Board P (1996) Chromosomal Localization of the Gene for the Human Theta Class Glutathione Transferase (GSTT1). Genomics 33: 121–123.
[18]
McIlwain C, Townsend D, Tew K (2006) Glutathione S-transferase polymorphisms: cancer incidence and therapy. Oncogene 25: 1639–1648.
[19]
Hayes JD, Flanagan JU, Jowsey IR (2005) Glutathione transferases. Annu Rev Pharmacol Toxicol 45: 51–88.
[20]
Zimniak P, Nanduri B, Piku？a S, Bandorowicz-Pikuls J, Singhal SS, et al. (2005) Naturally occurring human glutathione S-transferase GSTP1-1 isoforms with isoleucine and valine in position 104 differ in enzymic properties. Eur J Biochem 224: 893–899.
[21]
Hu X, Xia H, Srivastava SK, Herzog C, Awasthi YC, et al. (1997) Activity of four allelic forms of glutathione S-transferase hGSTP1–1 for diol epoxides of polycyclic aromatic hydrocarbons. Biochem Biophys Res Commun 238: 397–402.
[22]
Harries LW, Stubbins MJ, Forman D, Howard G, Wolf CR (1997) Identification of genetic polymorphisms at the glutathione S-transferase Pi locus and association with susceptibility to bladder, testicular and prostate cancer. Carcinogenesis 18: 641–644.
[23]
Wiesenhütter B, Selinski S, Golka K, Brüning T, Bolt HM (2007) Re-assessment of the influence of polymorphisms of phase-II metabolic enzymes on renal cell cancer risk of trichloroethylene-exposed workers. Int Arch Occup Environ Health 81: 247–251.
[24]
Ahmad ST, Arjumand W, Seth A, Saini AK, Sultana S (2012) Impact of glutathione transferase M1, T1, and P1 gene polymorphisms in the genetic susceptibility of North Indian population to renal cell carcinoma. DNA Cell Biol 31: 636–643.
[25]
Salinas-Sánchez AS, Sánchez-Sánchez F, Donate-Moreno MJ, Rubio-del-Campo A, Serrano-Oviedo L, et al. (2012) GSTT1, GSTM1, and CYP1B1 gene polymorphisms and susceptibility to sporadic renal cell cancer. Urol Oncol 30: 864–870.
[26]
Karami S, Boffetta P, Rothman N, Hung R, Stewart T, et al. (2008) Renal cell carcinoma, occupational pesticide exposure and modification by glutathione S-transferase polymorphisms. Carcinogenesis 29: 1567–1571.
[27]
？ori？ V, Plje？a-Ercegovac M, Mati？ M, Krivi？ B, ？uvakov S, et al. (2010) The role of GSTM1 and GSTT1 polymorphism in patients with renal cell carcinoma. J Medi Biochem 29: 204–210.
[28]
De Martino M, Klatte T, Schatzl G, Remzi M, Waldert M, et al. (2010) Renal cell carcinoma Fuhrman grade and histological subtype correlate with complete polymorphic deletion of glutathione S-transferase M1 gene. J Urol 183: 878–883.
[29]
Buzio L, De Palma G, Mozzoni P, Tondel M, Buzio C, et al. (2003) Glutathione S-transferases M1–1 and T1–1 as risk modifiers for renal cell cancer associated with occupational exposure to chemicals. Occup Environ Med 60: 789–793.
[30]
Sweeney C, Farrow DC, Schwartz SM, Eaton DL, Checkoway H, et al. (2000) Glutathione S-transferase M1, T1, and P1 polymorphisms as risk factors for renal cell carcinoma: a case-control study. Cancer Epidemiol Biomarkers Prev 9: 449–454.
[31]
Longuemaux S, Deloménie C, Gallou C, Méjean A, Vincent-Viry M, et al. (1999) Candidate Genetic Modifiers of Individual Susceptibility to Renal Cell Carcinoma A Study of Polymorphic Human Xenobiotic-metabolizing Enzymes. Cancer Res 59: 2903–2908.
[32]
Wang G, Hou J, Ma L, Xie J, Yin J, et al. (2011) Risk factor for clear cell renal cell carcinoma in Chinese population: A case–control study. Cancer Epidemiol36: 177–182.
[33]
Brüning T, Lammert M, Kempkes M, Thier R, Golka K, et al. (1997) Influence of polymorphisms of GSTM1 and GSTT1 for risk of renal cell cancer in workers with long-term high occupational exposure to trichloroethene. Arch Toxicol 71: 596–599.
[34]
Palli D, Saieva C, Luzzi I, Masala G, Topa S, et al. (2005) Interleukin-1 gene polymorphisms and gastric cancer risk in a high-risk Italian population. Am J Gastroenterol 100: 1941–1948.
[35]
Gao LB, Pan XM, Li LJ, Liang WB, Bai P, et al. (2011) Null genotypes of GSTM1 and GSTT1 contribute to risk of cervical neoplasia: an evidence-based meta-analysis. PloS one 6: e20157.
[36]
Higgins J, Thompson SG (2002) Quantifying heterogeneity in a meta-analysis. Statistics in medicine 21: 1539–1558.
[37]
Zintzaras E, Ioannidis J (2004) Heterogeneity testing in meta-analysis of genome searches. Genet Epidemiol 28: 123–137.
[38]
Egger M, Smith GD, Schneider M, Minder C (1997) Bias in meta-analysis detected by a simple, graphical test. Bmj 315: 629–634.
[39]
Begg CB, Mazumdar M (1994) Operating characteristics of a rank correlation test for publication bias. Biometrics: 1088–1101.
[40]
Ye Z, Song H, Higgins JPT, Pharoah P, Danesh J (2006) Five glutathione s-transferase gene variants in 23,452 cases of lung cancer and 30,397 controls: meta-analysis of 130 studies. PLoS Med 3: e91.
[41]
Liu R, Wang XH, Liu L, Zhou Q (2012) No association between the GSTM1 null genotype and risk of renal cell carcinoma: a meta-analysis. Asian Pac J Cancer Prev. 13(7): 3109–3112.
[42]
Cheng HY, You HY, Zhou TB (2012) Relationship between GSTM1/GSTT1 Null Genotypes and Renal Cell Carcinoma Risk: A Meta-Analysis. Renal Failure 34: 1052–1057.
[43]
Simic T, Savic-Radojevic A, Pljesa-Ercegovac M, Matic M, Mimic-Oka J (2009) Glutathione S-transferases in kidney and urinary bladder tumors. Nat Rev Urol 6: 281–289.
[44]
van Bladeren PJ (2000) Glutathione conjugation as a bioactivation reaction. Chem Biol Interact 129: 61–76.
[45]
Groves CE, Lock EA, Schnellmann RG (1991) Role of lipid peroxidation in renal proximal tubule cell death induced by haloalkene cysteine conjugates. Toxicol Appl Pharmacol 107: 54–62.
[46]
Dekant W, Vamvakas S, Berthold K, Schmidt S, Wild D, et al. (1986) Bacterial β-lyase mediated cleavage and mutagenicity of cysteine conjugates derived from the nephrocarcinogenic alkenes trichloroethylene, tetrachloroethylene and hexachlorobutadiene. Chem Biol Interact 60: 31–45.
[47]
Pekmezovi？ T (2010) Gene-environment interaction: A genetic-epidemiological approach. JAMA 29: 131–134.
