Gene deletion and partial deficiency of the glutathione <i>S</i>‐transferase (ligandin) system in man

Board, P.G.

doi:10.1016/0014-5793(81)80933-7

Cited by 47 publications

(21 citation statements)

References 11 publications

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“…There are four subclasses in mammalian cells, Alpha, Mu, Pi and Theta (Mannervik et al, 1992). The M1 member of the mu subclass is poly-morphic, being expressed in only 50-60% of Caucasians because of a gene deletion on the 'null' allele (Board et al, 1981a;1981b;Seidegard et al, 1988). Previous studies have shown that the homozygous null genotype is more common among patients with colorectal cancer (Strange et al, 1991;Zhong et al, 1993), squamous cell carcinoma of the lung (Hirvonen et al, 1993), and other lung cancers (Seidegard et al ., 1990;Kihara et al ., 1993).…”

Section: Introductionmentioning

confidence: 99%

Polymorphism of the CYP1A1 and glutathione-S-transferase gene in Korean lung cancer patients

Hong

Chang²,

Kwon³

et al. 1998

Exp Mol Med

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The levels of expressions and catalytic activities of cytochrome P450 (CYP1A1) and glutathione-S-t r a n sferase class (GSTM1) enzymes in lungs and their metabolic balance may be an important determinant host factor underlying lung cancer. Genetic differences in metabolism, MspI restriction sites, Ile-Val polymorphism of CYP1A1 gene, and the null genotype of GSTM1 have been reported to be associated with susceptibility to lung cancer. The present studies were undertaken to establish frequencies of the polymorphic genotypes of CYP1A1 and GSTM1 in Koreans, and to evaluate linkage disequilibrium of the genotypes associated with higher lung cancer risks among Koreans. GSTM1(-) genotype was found in 52% of control subjects, whereas it was found in 55% of lung cancer patients. The allelic variants in CYP1A1 were distributed differently in lung cancer patients and controls. The heterozygous genotype frequency of the MspI site in lung cancer patients (53%) was higher than in controls (49%). The frequency of Ile/Val genotype of CYP1A1 was low in lung cancer patients, which are mostly squamous cell carcinoma.

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Section: Introductionmentioning

confidence: 99%

Polymorphism of the CYP1A1 and glutathione-S-transferase gene in Korean lung cancer patients

Hong

Chang²,

Kwon³

et al. 1998

Exp Mol Med

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“…Three genetic loci encoding human liver GT isoenzymes have been characterized: GSTJ, GST2, and GST3 (8)(9)(10). GSTJ corresponds to the class-mu isoenzyme, GST2 corresponds to the class-alpha isoenzyme, and GST3 encodes the placental class-pi GT (3,11).…”

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confidence: 99%

“…GSTJ corresponds to the class-mu isoenzyme, GST2 corresponds to the class-alpha isoenzyme, and GST3 encodes the placental class-pi GT (3,11). The GSTI locus is polymorphic in human populations and displays three alleles: GSTJ-O (null), GSTI-1, and GSTJ-2 (8)(9)(10)12). Studies on Indian,…”

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confidence: 99%

Hereditary differences in the expression of the human glutathione transferase active on trans-stilbene oxide are due to a gene deletion.

Seidegård

Vorachek

Pero

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

624

301

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Glutathione transferase (GT; EC 2.5.1.18) mRNA levels were measured in human liver samples by using mouse and human cDNA clones that encode class-mu and class-alpha GT. Although all the RNA samples examined contained class-alpha GT mRNA, class-mu GT mRNA was found only in individuals whose peripheral leukocytes expressed GT activity on the substrate trans-stilbene oxide. The mouse class-mu cDNA clone was used to identify a human class-mu GT cDNA clone, AGTH411. The amino acid sequence of the GT encoded by AGTH411 is identical with the 23 residues determined for the human liver GT-I isoenzyme and shares 76-81% identity with mouse and rat class-mu GT isoenzymes. The mouse and human class-mu GT cDNA inserts hybridize with multiple BamHI and EcoRI restriction fragments in the human genome. One of these hybridizing fragments is missing in the DNA of individuals who lack GT activity on trans-stilbene oxide. Hybridizations with nonoverlapping subfragments of AGTH411 suggest that there are at least three class-mu genes in the human genome. One of these genes appears to be deleted in individuals lacking GT activity on trans-stilbene oxide.The glutathione transferases (GTs, EC 2.5.1.18) are a family of catalytic and binding proteins that detoxify chemical carcinogens (1,2). Multiple GT isoenzymes have been isolated from human, rat, and mouse tissues (2). Protein sequence data and antibody cross-reactivity have been used to group these isoenzymes into three distinct classes that have been termed alpha, mu, and pi (3). Members of the same class share 75-95% amino acid sequence identity, whereas members of different classes share 25-30% sequence identity. Livers of all adult humans express several class-alpha GTs; in addition, the livers of about one-half of the adult population contain a class-mu isoenzyme, p (3,4). The GT-p. isoenzyme has been shown to be similar or identical to a GT activity against trans-stilbene oxide (GT-tSBO) that is measured in peripheral leukocytes (5). Studies on several hundred subjects have shown a large variation in GT-tSBO activity among individuals; -50% of the population lacks GT-tSBO activity (6). Individuals lacking GT-tSBO are more likely to contract lung cancer (7).Three genetic loci encoding human liver GT isoenzymes have been characterized: GSTJ, GST2,. GSTJ corresponds to the class-mu isoenzyme, GST2 corresponds to the class-alpha isoenzyme, and GST3 encodes the placental class-pi GT (3, 11). The GSTI locus is polymorphic in human populations and displays three alleles: GSTJ-O (null), GSTI-1, and GSTJ-2 (8-10, 12). Studies on Indian,Chinese, and Caucasian populations have shown that the fraction of the population with two null GSTJ alleles ranges from 31% to 66% (8,12). The polymorphism at the GSTI locus is similar to the variation in GT-tSBO activity and is consistent with the observation that the GSTI locus encodes the GT-p. isoenzyme (J.S., unpublished data) that is responsible for GT-tSBO activity (5). Three additional human loci have been described: GST4, GST5, and GST6 (1...

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“…Polymorphisms: The restriction mapping data revealed the presence of a GST mu cluster with two GSTM1 genes in tandem situated between the GSTM2 and GSTM5 genes (McLellan et al, 1997). The GSTM1 gene contains four different alleles, leading to several M1 class polymorphisms, designated as GSTM1-0, GSTM1-A, GSTM1-B and GSTM1-1x2 alleles (Wu et al, 2012;Board PG, 1981). GSTM1-0 (GSTM1 null allele) arose from a recombination event during evolution between 2 highly homologous regions flanking this locus, resulting in deletion of a 20-kb segment (Xu et al, 1998).…”

Section: Descriptionmentioning

confidence: 99%

GSTM1 (Glutathione S-transferase M1)

Plješa-Ercegovac¹,

Matić²

2017

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Gene deletion and partial deficiency of the glutathione S‐transferase (ligandin) system in man

Cited by 47 publications

References 11 publications

Polymorphism of the CYP1A1 and glutathione-S-transferase gene in Korean lung cancer patients

Polymorphism of the CYP1A1 and glutathione-S-transferase gene in Korean lung cancer patients

Hereditary differences in the expression of the human glutathione transferase active on trans-stilbene oxide are due to a gene deletion.

GSTM1 (Glutathione S-transferase M1)

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