|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Thus, gene therapy of human oral cancer by increasing the expression of MnSOD activity in target cells might be used to prevent or reduce human oral tumor malignancy.
|
9095410 |
1997 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
MnSOD is reduced in a variety of tumor types and has been proposed to be a new kind of tumor suppressor gene, but the mechanism(s) by which MnSOD suppresses malignancy is unclear.
|
10919671 |
2000 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
Reconstitution of MnSOD expression in several human cancer cell lines leads to reversion of malignancy and induces a resistant phenotype to the cytotoxic effects of TNF and hyperthermia.
|
11165872 |
2001 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Reconstitution of MnSOD expression in several human cancer cell lines leads to reversion of malignancy and induces a resistant phenotype to the cytotoxic effects of TNF and hyperthermia.
|
11165872 |
2001 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
Reconstitution of MnSOD expression in several human cancer cell lines leads to reversion of malignancy and induces a resistant phenotype to the cytotoxic effects of TNF and hyperthermia.
|
11165872 |
2001 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
A family of AP-2 proteins down-regulate manganese superoxide dismutase expression.
|
11278550 |
2001 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
A family of AP-2 proteins down-regulate manganese superoxide dismutase expression.
|
11278550 |
2001 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
We therefore examined if polymorphism in the mitochondrial targeting sequence of the MnSOD gene modified individual susceptibility to this malignancy or related asbestos-associated pulmonary disorders.
|
11849743 |
2002 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
These findings, coupled with our previous observation that several cancer cell lines have mutations in the promoter region of the human MnSOD gene, which lead to an increase in an AP-2-binding site and a decrease in the promoter activity, signal the importance of understanding the promoter structure and the regulation of the human SOD2 gene by Sp1 and AP-2.
|
11853549 |
2002 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
These findings, coupled with our previous observation that several cancer cell lines have mutations in the promoter region of the human MnSOD gene, which lead to an increase in an AP-2-binding site and a decrease in the promoter activity, signal the importance of understanding the promoter structure and the regulation of the human SOD2 gene by Sp1 and AP-2.
|
11853549 |
2002 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
Tamoxifen enhancement of TNF-alpha induced MnSOD expression: modulation of NF-kappaB dimerization.
|
12032862 |
2002 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
Tamoxifen enhancement of TNF-alpha induced MnSOD expression: modulation of NF-kappaB dimerization.
|
12032862 |
2002 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
In addition, the wide variation in Mn-SOD and MT mRNA levels among normal subjects may reflect different susceptibilities to diseases including cancer.
|
14503839 |
2003 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
The antioxidant enzymes, glutathione peroxidase (GPx), catalase and superoxide dismutases (SOD1, SOD2), have altered expression patterns in these cancer cell lines.
|
15044326 |
2004 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
This study investigates the hypothesis that Mn-superoxide dismutase (MnSOD) influences cancer cell radiosensitivity by regulating the G(2)-checkpoint pathway.
|
16910775 |
2006 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
SOD2 is a key enzyme in the conversion of reactive oxygen species and has been implicated in a host of disease states, including cancer.
|
17192397 |
2007 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively.
|
17632733 |
2008 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
Treatment with both ZD55-MnSOD and 5-FU could induce more significant apoptosis in cancer cells compared with ZD55-MnSOD or 5-FU alone, respectively.
|
17632733 |
2008 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
A valine (Val) to alanine (Ala) substitution at amino acid 9, mapping within the mitochondrion-targeting sequence of the MnSOD gene, has been associated with an increased cancer risk.
|
18023606 |
2008 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
MnSOD gene polymorphism association with steroid-dependent cancer.
|
18553161 |
2009 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
The use of the G1677T polymorphism of SOD2 gene as a genetic risk marker may suggest new approaches for detection, prevention, treatment, and prognosis of cancer.
|
19405048 |
2009 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
CTD_human |
Complete sequencing and oxidative modification of manganese superoxide dismutase in medulloblastoma cells.
|
19676086 |
2009 |
|
Malignant Neoplasms
|
0.400 |
Therapeutic
|
group |
CTD_human |
Complete sequencing and oxidative modification of manganese superoxide dismutase in medulloblastoma cells.
|
19676086 |
2009 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Combination of the SOD2 gene silencing therapy and conventional radiotherapy should be attempted to improved cancer therapy for NPC.
|
20204285 |
2010 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Transgenic mice expressing a luciferase reporter gene under the control of the human MnSOD promoter demonstrate that the level of MnSOD is reduced prior to the formation of cancer.
|
20454814 |
2012 |