In vitro and In vivo Activity of the Nuclear Factor-κB Inhibitor Sulfasalazine in Human Glioblastomas
Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we demonstrated that the transcription factor nuclear factor (NF)-κB is constitutively activated in glioblastoma surgical samples, primary cultures, and c...
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| Published in | Clinical cancer research Vol. 10; no. 16; pp. 5595 - 5603 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article Web Resource |
| Language | English |
| Published |
Philadelphia, PA
American Association for Cancer Research
15.08.2004
American Association for Cancer Research, Inc. (AACR) |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis.
In this study, we demonstrated that the transcription factor nuclear factor (NF)-κB is constitutively activated in glioblastoma
surgical samples, primary cultures, and cell lines and promotes their growth and survival. Sulfasalazine, an anti-inflammatory
drug that specifically inhibits the activation of NF-κB, blocked the cell cycle and induced apoptosis in several glioblastoma
cell lines and primary cultures, as did gene therapy with a vector encoding a super-repressor of NF-κB. In vivo , sulfasalazine also significantly inhibited the growth of experimental human glioblastomas in nude mice brains. Given the
documented safety of sulfasalazine in humans, these results may lead the way to a new class of glioma treatment. |
|---|---|
| AbstractList | Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis.
In this study, we demonstrated that the transcription factor nuclear factor (NF)-κB is constitutively activated in glioblastoma
surgical samples, primary cultures, and cell lines and promotes their growth and survival. Sulfasalazine, an anti-inflammatory
drug that specifically inhibits the activation of NF-κB, blocked the cell cycle and induced apoptosis in several glioblastoma
cell lines and primary cultures, as did gene therapy with a vector encoding a super-repressor of NF-κB. In vivo , sulfasalazine also significantly inhibited the growth of experimental human glioblastomas in nude mice brains. Given the
documented safety of sulfasalazine in humans, these results may lead the way to a new class of glioma treatment. Abstract Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we demonstrated that the transcription factor nuclear factor (NF)-κB is constitutively activated in glioblastoma surgical samples, primary cultures, and cell lines and promotes their growth and survival. Sulfasalazine, an anti-inflammatory drug that specifically inhibits the activation of NF-κB, blocked the cell cycle and induced apoptosis in several glioblastoma cell lines and primary cultures, as did gene therapy with a vector encoding a super-repressor of NF-κB. In vivo, sulfasalazine also significantly inhibited the growth of experimental human glioblastomas in nude mice brains. Given the documented safety of sulfasalazine in humans, these results may lead the way to a new class of glioma treatment. Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we demonstrated that the transcription factor nuclear factor (NF)- Kappa B is constitutively activated in glioblastoma surgical samples, primary cultures, and cell lines and promotes their growth and survival. Sulfasalazine, an anti- inflammatory drug that specifically inhibits the activation of NF- Kappa B, blocked the cell cycle and induced apoptosis in several glioblastoma cell lines and primary cultures, as did gene therapy with a vector encoding a super- repressor of NF- Kappa B. In vivo, sulfasalazine also significantly inhibited the growth of experimental human glioblastomas in nude mice brains. Given the documented safety of sulfasalazine in humans, these results may lead the way to a new class of glioma treatment. Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we demonstrated that the transcription factor nuclear factor (NF)-kappaB is constitutively activated in glioblastoma surgical samples, primary cultures, and cell lines and promotes their growth and survival. Sulfasalazine, an anti-inflammatory drug that specifically inhibits the activation of NF-kappaB, blocked the cell cycle and induced apoptosis in several glioblastoma cell lines and primary cultures, as did gene therapy with a vector encoding a super-repressor of NF-kappaB. In vivo, sulfasalazine also significantly inhibited the growth of experimental human glioblastomas in nude mice brains. Given the documented safety of sulfasalazine in humans, these results may lead the way to a new class of glioma treatment. |
| Author | Peter M. Black Marie-Paule Merville Heddi Haddada Minh-Tuan Nguyen Khac Manuel Deprez Olivier Jolois Kadir Erkmen Marianne Bonif Mohamed Bentires-Alj Vincent Bours Pierre A. Robe Bernard Rogister |
| Author_xml | – sequence: 1 givenname: Pierre A surname: ROBE fullname: ROBE, Pierre A organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium – sequence: 2 givenname: Mohamed surname: BENTIRES-ALJ fullname: BENTIRES-ALJ, Mohamed organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium – sequence: 3 givenname: Peter M surname: BLACK fullname: BLACK, Peter M organization: Department of Neurosurgery, Children's Hospital, Harvard Medical School, Boston, Massachusetts, United States – sequence: 4 givenname: Vincent surname: BOURS fullname: BOURS, Vincent organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium – sequence: 5 givenname: Marianne surname: BONIF fullname: BONIF, Marianne organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium – sequence: 6 givenname: Bernard surname: ROGISTER fullname: ROGISTER, Bernard organization: Center for Molecular and Cellular Neurobiology, University of Liège, Liège, Belgium – sequence: 7 givenname: Manuel surname: DEPREZ fullname: DEPREZ, Manuel organization: Center for Molecular and Cellular Neurobiology, University of Liège, Liège, Belgium – sequence: 8 givenname: Heddi surname: HADDADA fullname: HADDADA, Heddi organization: Unité INSERM 487, Institut Gustave-Roussy, Villejuif, France – sequence: 9 givenname: Minh-Tuan surname: NGUYEN KHAC fullname: NGUYEN KHAC, Minh-Tuan organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium – sequence: 10 givenname: Olivier surname: JOLOIS fullname: JOLOIS, Olivier organization: Department of Histology, University of Liège, Liège, Belgium – sequence: 11 givenname: Kadir surname: ERKMEN fullname: ERKMEN, Kadir organization: Department of Neurosurgery, Children's Hospital, Harvard Medical School, Boston, Massachusetts, United States – sequence: 12 givenname: Marie-Paule surname: MERVILLE fullname: MERVILLE, Marie-Paule organization: Center for Cellular and Molecular Therapeutics, University of Liège, Liège, Belgium |
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| Cites_doi | 10.1006/excr.2001.5168 10.1215/15228517-4-4-261 10.1074/jbc.M203891200 10.1038/sj.onc.1203221 10.1016/S0142-9612(02)00013-3 10.1038/sj.onc.1203237 10.1074/jbc.M210631200 10.1002/1097-0142(19930415)71:8<2585::AID-CNCR2820710825>3.0.CO;2-S 10.1182/blood.V87.10.4340.bloodjournal87104340 10.1016/0092-8674(86)90346-6 10.1126/science.274.5288.782 10.3171/jns.2002.96.5.0909 10.1016/S0006-2952(00)00391-9 10.1210/me.9.4.401 10.1097/00001756-199611250-00049 10.2165/00003495-199550010-00009 10.1016/S0021-9258(17)37586-5 10.1172/JCI119848 10.1023/A:1022554824129 10.1038/sj.onc.1204535 10.1093/annonc/mdf165 10.1016/S0021-9258(17)31942-7 10.1074/jbc.M110480200 10.1038/sj.onc.1203239 10.1016/0003-2697(76)90527-3 10.1016/0304-3940(89)90090-6 10.1023/A:1015797713149 |
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| Keywords | Sulfanilamide derivatives Human Nervous system diseases Sulfonamide Glioblastoma Activity Malignant tumor In vitro Malignant glioma In vivo Central nervous system disease Sulfasalazine Inhibitor Transcription factor NFκB |
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| Snippet | Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis.
In this study, we... Abstract Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we... Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis. In this study, we... |
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| SubjectTerms | Anti-Inflammatory Agents, Non-Steroidal/toxicity Antineoplastic Agents Biological and medical sciences Brain Neoplasms/drug therapy/pathology Cell Line, Tumor Gene Therapy Glioblastoma/drug therapy/pathology Human health sciences Humans Medical sciences Neurologie Neurology NF-kappa B/antagonists & inhibitors Pharmacology. Drug treatments Sciences de la santé humaine Sulfasalazine/toxicity Tumor Cells, Cultured Tumors |
| Title | In vitro and In vivo Activity of the Nuclear Factor-κB Inhibitor Sulfasalazine in Human Glioblastomas |
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