Expression of Nuclear Factor-kB, Tumor Necrosis Factor Receptor Type 1, and c-Myc in Human Astrocytomas
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概要
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Tumor necrosis factor receptor type 1 (TNFR1) and c-Myc are important in signal transduction in tumor necrosis factor-α (TNF-α)-induced cytotoxicity, whereas activation of nuclear factor-kB (NF-kB) protects against TNF-α-induced apoptosis. This study investigated the expression of NF-kB, TNFR1, and c-Myc in human astrocytoma tissues by reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemical analysis. TNFR1 messenger ribonucleic acid (mRNA) and c-Myc mRNA were frequently expressed in malignant astrocytomas, especially in glioblastomas, compared with low-grade astrocytomas by PCR analysis. TNFR1 and c-Myc mRNAs were barely detectable in normal brain tissues. NF-kB p50 and p65 subunit mRNAs were detected in various grades of astrocytomas, with frequent expression in malignant astrocytomas. The presence of activated NF-kB was confirmed by nuclear localization in neoplastic astrocytes as determined by immunohistochemistry. Both p50 and p65 subunits were inhomogeneously expressed in neoplastic astrocytes of glioblastoma, but only in a few scattered tumor cells in low-grade astrocytoma, and almost undetectable in normal brain tissues. These results indicate that TNFR1 and c-Myc are overexpressed in malignant astrocytomas, and this may increase the cellular sensitivity to the cytotoxic action of TNF-α. NF-kB p50 and p65 were simultaneously induced and activated in malignant astrocytomas. Our results suggest that the constitutive activation of NF-kB subunits in malignant astrocytoma, especially in glioblastoma, could be associated with the resistance to TNF-α immunotherapy, and indicates new therapeutic strategies for malignant astrocytomas.
- 日本脳神経外科学会の論文
- 2001-04-15
著者
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OHSHIMA Koichi
Department of Pathology, Kurume University School of Medicine
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Fukushima Takeo
Departments of Neurosurgery, Faculty of Medicine, Fukuoka University
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HAYASHI Shuji
Department of Safety Assessment, Fuji Gotemba Research Laboratory, Chugai Pharmaceutical Co., Ltd.
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UENO Yushi
Department of Neurosurgery, Fukuoka University Faculty of Medicine
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YAMAMOTO Masaaki
Department of Neurosurgery, Fukuoka University School of Medicine
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Ueno Yushi
Department Of Neurosurgery Fukuoka University Faculty Of Medicine
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Ueno Yushi
Department Of Neurosurgery Fukuoko University School Of Medicine
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IKEDA Kohichi
Department of Neurosurgery, Fukuoko University School of Medicine
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SOMA Gen-Ichiro
Institute for Health Sciences, Tokushima Bunri University
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Ikeda Kohichi
Department Of Neurosurgery Fukuoko University School Of Medicine
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Hayashi Shuji
Department Of Neurosurgery Fukuoka University Faculty Of Medicine
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Hayashi Shuji
Department Of Neurosurgery Fukuoko University School Of Medicine
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Fukushima Takeo
Department Of Neurosurgery Fukuoko University School Of Medicine
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Fukushima Takeo
Department Of Neurosurgery Fukuoka University
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Soma Gen-ichiro
Institute For Health And Sciences Tokushima Bunri University
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Soma Gen-ichiro
Institute For Health Sciences Tokushima Bunri University
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Yamamoto Masaaki
Department Of Medicine Institute Of Clinical Endocrinology Tokyo Women's Medical University
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Ohshima Koichi
Department Of Pathology Fukuoko University School Of Medicine
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Ohshima Koichi
Department Of First Pathology Fukuoka University
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Yamamoto Masaaki
Department Of Neurosurgery Fukuoko University School Of Medicine:molecular Oncology Center Fukuoko U
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Fukushima Takeo
Department Of Neurosurgery Faculty Of Medicine Fukuoka University
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Ohshima Koichi
Department Of Cell Pathology Graduate School Of Medical Sciences Kumamoto University
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Yamamoto Masaaki
Department Of Dermatology Hyogo College Of Medicine
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Yamamoto Masaaki
Department of Chemistry, Faculty of Science, Kanazawa University
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Hayashi Shuji
Department of Cardiovascular Medicine, Tokushima University Hospital, Japan
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