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superoxide dismutase/rinnavähk

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BACKGROUND Defects of manganese superoxide dismutase (MnSOD) have long been implicated in generation of oxidative stress and risk susceptibility to various cancers. Two functional polymorphisms within the MnSOD gene, including the Val-9Ala of the mitochondrial targeting sequence (MTS) and the
The manganese superoxide dismutase (MnSOD) ala16val polymorphism has been associated with various diseases including breast cancer. In the present study, we investigated levels of MnSOD protein, enzymatic activity, and mRNA with respect to MnSOD genotype in several human breast carcinoma cell lines

Superoxide dismutases and p53 protein levels in blood cells of breast cancer patients.

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OBJECTIVE Radiation treatment of breast cancer (BC) often results in post-therapy complications. The undesired sequelae could be avoided by the diagnostic screening of biomarkers for prediction of ionizing radiation (IR)-linked injury of healthy tissues. METHODS The expression of antioxidative
Human manganese containing superoxide dismutase (MnSOD) cDNA was transfected into a human breast cancer cell line (MCF-7) in order to examine the effect of increased functional MnSOD on the cellular phenotype. A MnSOD-overexpressing clone was compared to control vector-transfected cells and to wild

[Expression of superoxide dismutase 2 in breast cancer and its clinical significance]

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Objective: To evaluate the expression and prognostic value of superoxide dismutase 2 (SOD2) in breast cancer and explore its possible role in the occurrence and progression of breast cancer. Methods:
This study was designed to examine the role superoxide production by macrophages plays in tumor killing. When superoxide dismutase was added to the normal macrophage-tumor cell (MA-160 cell line) suspensions macrophage mediated tumor cytotoxicity was suppressed. In contrast, superoxide dismutase
Manganese superoxide dismutase (MnSOD) is known to play a role in cancer. MnSOD exerts a tumor suppressive effect in estrogen-dependent human breast cancer cells. In the present study we investigated the in vitro role of MnSOD in the growth of some aggressive and highly metastatic

Association between manganese superoxide dismutase (MnSOD) gene polymorphism and breast cancer risk.

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Superoxide dismutases play a key role in the detoxification of superoxide radicals and thus protect cells from damage induced by free radicals. Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species. Polymorphism in the
BACKGROUND studies show changes in zinc metabolism in women with breast cancer. This mineral has antioxidant action, and disorders in its biochemical parameters are related to poor prognosis of the disease and increase in the carcinogenic process. OBJECTIVE this study evaluated the activity of
BACKGROUND Manganese superoxide dismutase (MnSOD) inhibits oxidative damage and cancer therapy effectiveness. A polymorphism in its encoding gene (SOD2: Val16Ala rs4880) may confer poorer breast cancer survival, but data are inconsistent. We examined the association of SOD2 genotype and breast
Anthracycline-based chemotherapy represents a milestone in the treatment of breast cancer. We previously demonstrated in an in vitro model that cyclin E overexpression is associated with increased expression of manganese superoxide dismutase (MnSOD) and resistance to doxorubicin. In the present

Polymorphism in the manganese superoxide dismutase (MnSOD) gene and risk of breast cancer in young women.

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OBJECTIVE Manganese superoxide dismutase (MnSOD) is one of the major enzymes implicated in the cellular defence against reactive oxygen species. Low expression of MnSOD has been observed in different cancer tissues and several reports have shown that overexpression of MnSOD inhibits growth in
Disturbances in redox regulation are suggested to be involved in the development of breast cancer. We conducted a hospital-based case-control study to examine the hypothesis that lower plasma antioxidant concentration is related to higher risk of breast cancer and that genetic polymorphism of
OBJECTIVE Small proportions of patients receiving radiotherapy develop marked long-term radiation damage. It is thought that this is due, at least in part, to intrinsic differences in cellular radiosensitivity, but the underlying mechanism is unknown. Reactive oxygen species are involved in cellular

Overexpression of manganese or copper-zinc superoxide dismutase inhibits breast cancer growth.

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We have studied the effects of overexpression of superoxide dismutase (SOD), a tumor suppressor protein that dismutes superoxide radical to H2O2, on breast cancer cell growth in vitro and xenograft growth in vivo. No previous work has directly compared the growth-suppressive effects of manganese SOD
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