Polymorphisms of glutathione S -transferase genes ( GSTM1 , GSTP1 and GSTT1 ) and bladder cancer susceptibility in the Turkish population

Toruner, Gokce; Akyerli, Cemaliye Boylu; Uçar, Ahmet; Aki, Tuncay; Atsü, Necmettin; Özen, Haluk; Tez, Mesut; Çetinkaya, Mesut; Özçelık, Tayfun

doi:10.1007/s002040100268

Cited by 71 publications

(49 citation statements)

References 21 publications

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“…We found ever smokers with a 2.5 fold more risk of bladder cancer with twice higher heterozygote frequency in cases than in controls (27% versus 13.4%: p>0.05). Similar sort of results are shared by many studies confirming smoking as risk factor in GSTP1 A>G polymorphism (Törüner 2001;Rama et al, 2005). Significant association of bladder carcinoma increased with patients >50 years of age with OR 2.50 (0.89-6.98), consistent with other studies (Brauers et al, 2000: Coa et al, 2005.…”

Section: From Caucasians and Coa Et Al (2005)supporting

confidence: 77%

GSTP1 Gene Ile105Val Polymorphism Causes an Elevated Risk for Bladder Carcinogenesis in Smokers

Pandith

Lateef²,

Shahnawaz³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: The glutathione S transferase (GST) family of enzymes plays a vital role in the phase II biotransformation of environmental carcinogens, pollutants, drugs and other xenobiotics. GSTs are polymorphic and polymorphisms in GST genes have been associated with cancer susceptibility and prognosis. GSTP1 is associated with risk of various cancers including bladder cancer. A case control study was conducted to determine the genotype distribution of GSTP1 A>G SNP, to elucidate the possible role of this SNP as a risk factor in urinary bladder cancer (UBC) development and to examine its correlation with clinico-pathologic variables inUBC cases. Materials and Methods: Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) approach, we tested the genotype distribution of 180 bladder cancer patients in comparison with 210 cancer-free controls from the same geographical region with matched frequency in age and gender. Results: We did not observe significant genotype differences between the control and bladder cancer patients overall with an odds ratio (OR)=1.23 (p>0.05). The rare allele (AG+GG) was found to be present more in cases (28.3%) than in controls (24%), though the association was not significant (p<0.05). However, a significant risk of more than 2-fold was found for the variant allele (AG+GG) with smokers in cases as compared to controls (p>0.05). Conclusions: Thus, it is evident from our study that GSTP1 SNP is not implicated overall in bladder cancer, but that the rare, valine-related allele is connected with higher susceptibility to bladder cancer in smokers and also males.

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Section: From Caucasians and Coa Et Al (2005)supporting

confidence: 77%

GSTP1 Gene Ile105Val Polymorphism Causes an Elevated Risk for Bladder Carcinogenesis in Smokers

Pandith

Lateef²,

Shahnawaz³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Ma jo rity of the stu di es investigating the re la ti on bet we en blad der can cer and GSTM1 ha ve re por ted an in crea sed risk when there is a lack of GSTM1 ac tivity. 29,30 In cre a sed GST ac ti vity in uri nary blad der can cer pa ti ents may be a re sult of up-re gu la ti on of GST ge ne du ring the car ci no ge ne sis. Al ter na ti vely, this in cre a se may be a cel lu lar adap ti ve res pon se or de fen se mec ha nism aga inst ma lig nant trans for mati on.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of 8-Hydroxy-2\'-Deoxyguanosine Concentration and Antioxidant Enzyme Activities in Bladder Cancer Patients

Dinçer¹,

Akçay²,

Kural³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Oxi dant/an ti o xi dant ba lan ce has be en sug ges ted as an im por tant fac tor for ini ti a ti on and prog res si on of can cer. The pur po se of this study was to exa mi ne 8-hydroxy-2'-deoxy gu a no si ne (8-OHdG) le vel which is a mar ker of oxi da ti ve DNA da ma ge, su pe ro xi de dis mu ta se (SOD), glu tat hi o ne pe ro xi da se (GPx) and glu tat hi o ne S-trans fe ra se (GST) ac ti vi ti es as an ti o xi dant enz ymes, in se rum of uri nary blad der can cer, and to de ter mi ne re la ti ons bet we en me a su red pa rame ters and tu mor cha rac te ris tics such as his to lo gi cal gra de, lo cal in va si on and tu mor si ze. M Ma a t te e r ri i --a al l a an nd d M Me et t h ho od ds s: : Forty pa ti ents with uri nary blad der can cer we re inc lu ded in the study. Blo od samp les we re col lec ted just be fo re the re sec ti on. Se rum le vels of 8-OHdG we re me a su red with a com pe ti ti ve ELI SA kit, SOD and GPx ac ti vi ti es we re me a su red by spec trop ho to met ric kits, GST ac ti vity was de ter mi ned by spec trop ho to met ric as say. R Re e s su ul lt ts s: : The re was no sig ni fi cant dif fe ren ce bet we en pa ti ent and con trol gro ups for se rum 8-OHdG le vel and GPx ac ti vity. Ho we ver se rum SOD ac ti vity was sig ni fi cantly lo wer (P< 0.001) and GST ac ti vity was sig ni fi cantly hig her (P< 0.001) in the pa ti ent gro up as com pa red to con trol gro up. Tu mor si ze fo und to be ne ga ti vely cor re la ted with GST ac ti vity (r: -0.43, P< 0.01). C Co on nc c l lu u s si i o on n: : Da ta show that se rum le vel of 8-OHdG does not have a prog nos tic po ten ti al for uri nary blad der can cer. An ti o xi dant ba lan ce is dis tur bed in the se pati ents however chan ges in an ti o xi dant enz yme ac ti vi ti es does not have a prog nos tic va lu e. The most pro mi sing an ti o xi dant enz yme is GST be ca u se of its ne ga ti ve as so ci a ti on with tu mor si ze.K Ke ey y W Wo or rd ds s: : Glu tat hi o ne pe ro xi da se; su pe ro xi de dis mu ta se; glu tat hi o ne trans fe ra se; 8-hydroxy-2'-de oxy gu a no si ne; uri nary blad der ne op lasms Ö ÖZ ZE ET T A Am ma aç ç: : Ok si dan/an ti ok si dan den ge nin kan ser olu şu mu ve iler le me sin de önem li bir fak tör ol du ğu ile ri sü rül mek te dir. Bu ça lış ma nın ama cı me sa ne kan ser li has ta lar da se rum da DNA ok sidas yo nu be lir te ci olan 8-hid rok si-2'-de ok si gu a no zin (8-OHdG) dü ze yi ile an ti ok si dan ak ti vi te ola rak sü pe rok sit dis mu taz (SOD), glu tat yon pe rok si daz (GPx) ve glu tat yon S-trans fe raz (GST) ak ti vi te le ri ni ölç mek ve bu pa ra met re le rin his to lo jik gra de, lo kal in vaz yon, tü mör bü yük lü ğü gibi tü mör ka rak te ris tik le ri ile iliş ki le ri ni be lir le mek tir. G Ge e r re eç ç v ve e Y Yö ön n t te em m l le er r: : Me sa ne kan ser li 40 has ta ça lış ma kap sa mı na alın dı. Kan ör nek le ri ame li ya tın he men ön ce sin de top lan dı. Se rum 8-OHdG dü zey le ri ya rış ma lı ELI ...

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“…The summary should not be regarded as a representative review of the literature. Further details and references to original sources can be found in reviews [4,6,7] and in the references quoted in more recent accounts [26,[44][45][46][47]. 2 The risks quoted are the odds ratios associated with the specified alleles.…”

Section: T1mentioning

confidence: 99%

Detoxification of electrophilic compounds by glutathione S‐transferase catalysis: Determinants of individual response to chemical carcinogens and chemotherapeutic drugs?

2003

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Abstract. The glutathione S-transferases (GSTs) catalyze the GSH-dependent detoxification of reactive electrophiles such as genotoxic chemical carcinogens and cytotoxic chemotherapeutic agents. Allelic polymorphism in the GSTs has been used to investigate the hypothesis that GSTs are involved in susceptibility to human cancers. Such studies have resulted in low penetrance, high prevalence associations between cancer risk and GST polymorphisms. By examination of interindividual variation of GST expression it becomes clear that GST genotype alone is not an accurate predictor of GST expression. GST expression is tissue specific and interindividual variation of expression is at least 7-fold in normal tissues. Thus, populations of the same genotype are actually heterogeneous as regards expression. Similarly, polymorphisms are not effective in all tissues and GST induction is not independent of genotype. Mechanistic models for chemical aspects of colorectal cancer and chemotherapy for breast cancer demonstrate some of the ways by which such interactions can be studied and the potential for future studies.

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Polymorphisms of glutathione S -transferase genes ( GSTM1 , GSTP1 and GSTT1 ) and bladder cancer susceptibility in the Turkish population

Cited by 71 publications

References 21 publications

GSTP1 Gene Ile105Val Polymorphism Causes an Elevated Risk for Bladder Carcinogenesis in Smokers

GSTP1 Gene Ile105Val Polymorphism Causes an Elevated Risk for Bladder Carcinogenesis in Smokers

Evaluation of 8-Hydroxy-2\'-Deoxyguanosine Concentration and Antioxidant Enzyme Activities in Bladder Cancer Patients

Detoxification of electrophilic compounds by glutathione S‐transferase catalysis: Determinants of individual response to chemical carcinogens and chemotherapeutic drugs?

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