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thyroid neoplasms/glutathione
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Seite 1 von 65 Ergebnisse
Comparative analysis of the prevalence of the glutathione S-transferase (GST) system in malignant and benign thyroid tumor cells.
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OBJECTIVE
When null, the mu and theta genes of the glutathione S-transferase system (GSTM1 and GSTT1, respectively) are related to malignant tumors affecting the lungs, colon, prostate, bladder and head and neck. In the thyroid, the appearance of cancer has been correlated with deletion of these
The null genotype of glutathione s-transferase M1 and T1 locus increases the risk for thyroid cancer.
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Susceptibility to chemical carcinogens plays an important role in the development of most cancers. Several polymorphisms of human drug-metabolizing enzymes influence this individual susceptibility. The genes that encode the isoenzymes of the glutathione s-transferase (GST) system present a
Glutathione S-transferase M1, T1, and P1 polymorphisms and thyroid cancer risk: a meta-analysis.
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Glutathione S-transferases (GSTs) genetic variants have been explored extensively as a predictive factor for cancer etiology. This meta-analysis aimed to examine the associations GSTM1, GSTT1, and GSTP1 genetic polymorphisms with thyroid cancer risk. PubMed, EMBASE, Cochrane Library, and HuGNet
[Transferase S-glutathione class pi gene (GSTP1) polymorphism in thyroid cancer patients].
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BACKGROUND
One of the potential genes which can increase the risk of cancer is GSTP1 gene. It encodes enzyme called glutathione S-transferase pi class, which is involved in the detoxification of a variety of potential carcinogenic compounds. Polymorphism in this gene can cause the amino acid
Combined effects of glutathione S-transferase polymorphisms and thyroid cancer risk.
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Since exposure to ionizing radiation, a risk factor for thyroid cancer, may produce genotoxins potentially eliminated by glutathione-S-transferases, we conducted a case control study to evaluate the role of the GSTM1- and GSTT1-null genotypes and GSTP1 polymorphisms in thyroid cancer. The frequency
Glutathione S-transferase polymorphisms in thyroid cancer patients.
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Glutathione S-transferases (GST) are enzymes involved in the metabolism of many carcinogens and mutagens, also acting as important free-radical scavengers. The existence of different genetic polymorphisms in human populations has proven to be a susceptibility factor for different tumours.
Glutathione peroxidase 3 gene polymorphisms and risk of differentiated thyroid cancer.
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BACKGROUND
The antioxidant enzyme glutathione peroxidase 3 (GPX3) can lessen the oxidative stress in the thyroid gland. We tested for the association between tagging single nucleotide polymorphisms (tSNPs) of the GPX3 gene and the risk of differentiated thyroid cancer (DTC).
METHODS
A total of 6
Polymorphisms of methylenetetrahydrofolate reductase and glutathione S-transferase are not associated with the risk of papillary thyroid cancer in Korean population.
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Korea has the highest incidence of thyroid cancer of any nation. We conducted a population-based, case-control study of the association between the risk of papillary thyroid cancer (PTC) in the Korean population and polymorphisms of methylenetetrahydrofolate reductase (MTHFR) C677T, glutathione
A possible role for selenoprotein glutathione peroxidase (GPx1) and thioredoxin reductases (TrxR1) in thyroid cancer: our experience in thyroid surgery.
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UNASSIGNED
Oxidative stress is responsible for some alterations in the chemical structure and, consequently, in the function of proteins, lipids, and DNA. Recent studies have linked oxidative stress to cancers, particularly thyroid cancer, but the mechanisms remain unclear. Here, we further
Role of oxidative stress and intracellular glutathione in the sensitivity to apoptosis induced by proteasome inhibitor in thyroid cancer cells.
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BACKGROUND
The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with conventional and other novel agents for the treatment of multiple myeloma (MM) and some solid cancers. Although bortezomib is known to be a selective proteasome inhibitor, the
Differentiated thyroid cancer and selenium supplements for protection of salivary glands from 131I treatment.
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Dear Editor, I read with great interest the article by Son et al about the radioprotective effect of selenium (Se) supplementation for the salivary glands from 131I treatment in patients with differentiated thyroid cancer (DTC). In this study, 8 patients received 300μg of Se (as inorganic sodium
Intracellular redox status controls spherogenicity, an in vitro cancer stem cell marker, in thyroid cancer cell lines.
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Cancer stem cells (CSCs), a small fraction of a tumor mass, are proposed to be highly crucial for cancer initiation, recurrence and metastasis. We have recently found that aldehyde dehydrogenase (ALDH) 1A3 is a CSC marker in some thyroid cancer cell lines, whose functional activity is, however, not
GSTT1 and M1 polymorphisms in Hürthle thyroid cancer patients.
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Glutathione S-transferases (GST) are an important part of cell defense against numerous genotoxic compounds and ROS. In order to test the possibility of association between the GSTT1 and M1 null allele variant, and the risk of TCO (thyroid carcinoma with cell oxyphilia), a case-control study was
Molecular prognosticators and genomic instability in papillary thyroid cancer.
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OBJECTIVE
Tumor progression has been attributed to the accumulation of DNA damage concurrent with selection of advantageous mutations; this DNA damage may result from failure to maintain genomic integrity or from susceptibility to carcinogens. Glutathione S-transferases (GSTs), enzymes that
Combined GSTM1 and GSTT1 null genotypes are associated with a lower risk of papillary thyroid cancer.
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Individual susceptibility to cancer is influenced by polymorphisms of genes encoding drug-metabolizing enzymes such as the glutathione S-transferases (GST). The null polymorphisms of the GSTM1 and GSTT1 genes have been associated to a modified risk of several cancers but studies of thyroid cancer
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