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glutathione/karcinom prsu

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Glutathione S-transferase P1 rs1695 A>G polymorphism and breast cancer risk: evidence from a meta-analysis.

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Přihlášení Registrace
Breast cancer (BC) is the most widespread cause of cancer-related deaths in women. Many published studies have assessed the association between the glutathione S-transferase P1 (GSTP1) rs1695 polymorphism and BC risk. However, the effect of the GSTP1 rs1695 polymorphism on BC risk has remained
Glutathione S-transferase M (GSTM) family is concerned with oxidative stress, which is associated with breast carcinogenesis and chemotherapy response. The null polymorphism of GSTM1 gene results in a thorough absence of the enzyme function. Our study was to evaluate the association between GSTM1

Glutathione S-transferases deletions may act as prognosis and therapeutic markers in breast cancer.

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Breast cancer (BC) is the main worldwide neoplasia in women. The metabolic balance between xenobiotic absorption and elimination rates plays an important role in preventing DNA damage and, consequently, tumor development. The glutathione S-transferases (GSTs), such as GSTM1 and GSTT1, and the

A comparative study of selenium concentration and glutathione peroxidase activity in normal and breast cancer patients.

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OBJECTIVE The present study was undertaken to compare plasma Se values and glutathione peroxidase (GPX) activity in normal and breast cancer patients. METHODS In a case-control study, forty-five breast cancer patients and the same number of healthy women were randomly selected from their population.

Reversal of hypermethylation and reactivation of glutathione S-transferase pi 1 gene by curcumin in breast cancer cell line.

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One of the mechanisms for epigenetic silencing of tumor suppressor genes is hypermethylation of cytosine residue at CpG islands at their promoter region that contributes to malignant progression of tumor. Therefore, activation of tumor suppressor genes that have been silenced by promoter methylation
Sodium butyrate (NaBu), a potent histone deacetylase inhibitor, modulates the expression of a large number of genes. The purpose of this study was to determine whether this dietary agent could induce apoptosis in MCF-7 cells, a breast cancer cell line that lacks caspase-3 activity, and to identify

Combined depletion of O6-alkylguanine-DNA alkyltransferase and glutathione to modulate nitrosourea resistance in breast cancer.

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MCF-7 human breast cancer cells possess high levels of O6-alkylguanine-DNA alkyltransferase and moderate levels of glutathione, and are more resistant to chloroethylnitrosoureas (CNUs) than cells with low levels of either molecule. The role of each as a component of CNU resistance was assessed using

Expression of p53, glutathione S-transferase-pi, and Bcl-2 proteins and benefit from adjuvant radiotherapy in breast cancer.

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BACKGROUND In clinical breast cancer research, the utility of certain biomarkers as predictors of response to surgery, chemotherapy, or hormonal therapy has been studied intensively. Much less research has been done on the relevance of biologic predictors of response to radiotherapy, which
Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer (BC) with higher metastatic rate and both local and systemic recurrence compared to non-TNBC. The generation of reactive oxygen species (ROS) secondary to oxidative stress is associated with DNA damage, chromosomal
OBJECTIVE Previous studies have indicated that RNA levels for pi-class glutathione S-transferase (GST pi), a phase II, drug-metabolizing enzyme, were inversely related to estrogen receptor (ER) and progesterone receptor (PR) levels in human breast tumors. Because GST pi also is expressed in normal

[Glutathione S-transferase M1 polymorphism and susceptibility to breast cancer in Chinese population: a meta-analysis].

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OBJECTIVE To evaluate the published data on association between present/null polymorphism of glutathione S-transferase M1 (GSTM1) and breast cancer risk in Chinese population in order to abttain a more precise and comprehensive estimation of the relationship. METHODS A meta-analysis was performed to

Radiation response of drug-resistant variants of a human breast cancer cell line: the effect of glutathione depletion.

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Two drug-resistant variants of the human breast cancer cell line MCF-7 have been shown previously to exhibit radiation resistance associated with an increase in the size of the shoulder on the radiation survival curve. In the present study, glutathione (GSH) depletion was achieved by exposure of

Impaired expression of glutathione peroxidase-4 gene in peripheral blood mononuclear cells: a biomarker of increased breast cancer risk.

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Breast cancer aetiology is unclear despite comprising approximately 28% of female cancers. Several risk factors are known. Not all women exhibiting established risk factors will develop breast cancer but many without recognised risk factors will, indicating involvement of unknown risk factors.

Glutathione S-transferase class mu deletion polymorphism and breast cancer: results from prevalent versus incident cases.

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A common deletion polymorphism in the gene coding for the glutathione S-transferase class mu (the GSTM1 gene) results in a decreased ability to detoxify carcinogenic epoxide intermediates and has been associated with increased breast cancer risk in some small studies. We studied the GSTM1 gene

Expression of glutathione S-transferase B1, B2, Mu and Pi in breast cancers and their relationship to oestrogen receptor status.

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The concentrations of glutathione S-transferase (GST) B1 and B2 (Alpha), Pi and Mu have been measured by radioimmunoassay in cytosols from 28 oestrogen receptor (ER) rich an 30 ER-poor breast tumours. GST B1, B2 and Pi was detected in all 58 breast tumour cytosols whilst GST Mu was found in only 28.
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