Human glutathione S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism

Pemble, Sally; Schroeder, Karsten; Spencer, Sharon R.; Meyer, David J.; Hallier, Ernst; Bolt, Hermann M.; Ketterer, Brian; Taylor, John B.

doi:10.1042/bj3000271

Cited by 1,160 publications

(629 citation statements)

References 25 publications

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“…On the other hand, frequent losses were observed in chromosomes 9p, 13q, 15q, 16q, 17q, and 22q. Except for 15q13.3 and 22q11.23 (containing GSTT1 gene locus, which might represent a germline polymorphism 17 ), most of these chromosomal losses were predominantly observed in the 'S' group of cases. Homozygous deletions were infrequent.…”

Section: Genomewide Copy Number Variationsmentioning

confidence: 99%

Genomewide copy number analysis of Müllerian adenosarcoma identified chromosomal instability in the aggressive subgroup

Lee

Changou

et al. 2016

Modern Pathology

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Müllerian adenosarcomas are malignant gynecologic neoplasms. Advanced staging and sarcomatous overgrowth predict poor prognosis. Because the genomic landscape remains poorly understood, we conducted this study to characterize the genomewide copy number variations in adenosarcomas. Sixteen tumors, including eight with and eight without sarcomatous overgrowth, were subjected to a molecular inversion probe array analysis. Copy number variations, particularly losses, were significantly higher in cases with sarcomatous overgrowth. Frequent gains of chromosomal 12q were noted, often involving cancer-associated genes CDK4 (six cases), MDM2, CPM, YEATS4, DDIT3, GLI1 (five each), HMGA2 and STAT6 (four), without association with sarcomatous overgrowth status. The most frequent losses involved chromosomes 13q (five cases), 9p, 16q and 17q (four cases each) and were almost limited to cases with sarcomatous overgrowth. MDM2 and CDK4 amplification, as well as losses of RB1 (observed in two cases) and CDKN2A/B (one case), was verified by FISH. By immunohistochemistry, all MDM2/CDK4-coamplified cases were confirmed to overexpress both encoded proteins, whereas all four cases with (plus an additional four without) gain of HMGA2 overexpressed the HMGA2 protein. Both cases with RB1 loss were negative for the immunostaining of the encoded protein. Chromothripsis-like copy number profiles involving chromosome 12 or 14 were observed in three fatal cases, all of which harbored sarcomatous overgrowth. With whole chromosome painting and deconvolution fluorescent microscopy, dividing tumor cells in all three cases were shown to have scattered extrachromosomal materials derived from chromosomes involved by chromothripsis, suggesting that this phenomenon may serve as visual evidence for chromothripsis in paraffin

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Section: Genomewide Copy Number Variationsmentioning

confidence: 99%

Genomewide copy number analysis of Müllerian adenosarcoma identified chromosomal instability in the aggressive subgroup

Lee

Changou

et al. 2016

Modern Pathology

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“…Genes encoding both proteins are colocalized on chromosome 22 and are separated by 50 kb (Pemble et al, 1994;Tan et al, 1995). Polymorphisms exist within both genes including a null phenotype (GSTT1*0) that exhibits decreased catalytic activity and has been associated with an increased risk of cancers of the head, neck and oral cavity (Strange and Fryer, 1999).…”

Section: Theta Classmentioning

confidence: 99%

Glutathione S-transferase polymorphisms: cancer incidence and therapy

2006

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The super family of glutathione S-transferases (GSTs) is composed of multiple isozymes with significant evidence of functional polymorphic variation. Over the last three decades, data from cancer studies have linked aberrant expression of GST isozymes with the development and expression of resistance to a variety of chemicals, including cancer drugs. This review addresses how differences in the human GST isozyme expression patterns influence cancer susceptibility, prognosis and treatment. In addition to the well-characterized catalytic activity, recent evidence has shown that certain GST isozymes can regulate mitogen-activated protein kinases or can facilitate the addition of glutathione to cysteine residues in target proteins (S-glutathionylation). These multiple functionalities have contributed to the recent efforts to target GSTs with novel small molecule therapeutics. Presently, at least two drugs are in latestage clinical testing. The evolving functions of GST and their divergent expression patterns in individuals make them an attractive target for drug discovery.

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“…GSTM1 and GSTT1 genes show genetic variability in humans. Up to 50% of the Caucasian population are null genotypes for the GSTM1 gene [56]. These null genotypes cannot conjugate metabolites specific for these enzymes, rendering these individuals more prone to damage caused by oxidative stress and possibly more susceptible to ARHL.…”

Section: Oxidative Stressmentioning

confidence: 99%

Ageing and hearing loss

Yan

2007

The Journal of Pathology

278

178

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Although many adults retain good hearing as they age, hearing loss associated with ageing is common among elderly persons. There are a number of pathophysiolological processes underlying age-related changes to functional components in the inner ear. Genetic factors determine the ageing process but are under the influence of intrinsic and environmental factors. It is difficult to distinguish changes of normal ageing from those of other contributing factors. The effects of age-related deafness can have significant physical, functional and mental health consequences. Although a deficit in hearing can be corrected to some degree by a hearing aid or other appropriate amplification devices, hearing-related rehabilitative needs are much more than simply amplifying external sound. Only by better understanding the process of ageing and its effect on the auditory function can we better accommodate elderly people in our day-to-day interactions. We review here the structure and function of the inner ear, pathophysiology associated with age-related hearing loss (ARHL), heritability, allelism and modifier genes of ARHL, and evaluate the genetic analyses for identification of genetic factors that are involved.

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Human glutathione S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism

Cited by 1,160 publications

References 25 publications

Genomewide copy number analysis of Müllerian adenosarcoma identified chromosomal instability in the aggressive subgroup

Genomewide copy number analysis of Müllerian adenosarcoma identified chromosomal instability in the aggressive subgroup

Glutathione S-transferase polymorphisms: cancer incidence and therapy

Ageing and hearing loss

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