| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
Fas/APO-1 (CD95) is a cell surface receptor that mediates apoptosis when it reacts with Fas ligand (FasL) or Fas antibody. I previously reported that Fas expression in predominantly induced in perinecrotic glioma cells, suggesting that Fas induction is associated with apoptosis and necrosis formation, a histological hallmark of glioblastomas. Cysteine proteases of caspase family {interleukin-1 beta-converting enzyme (ICE)} have been implicated as components of cell death pathway and have been reported to involved in Fas, chemotherapeutic agents, and radiation-induced apoptosis. In this study, I assessed the expression lf FasL,ICE,ICE/CED-3 homologue-IL (ICH-1), and CPP32/Yama/apopain in 13 cases of primary astrocytic brain tumors (two low grade astrocytomas, five anaplastic astrocytomas, and six glioblastomas) by reverse transcription (RT) -PCR,Western blot analysis, and immunohistochemistry. RT-PCR revealed that all astrocytic brain tumors express FasL.Immunohistochemically, FasL was predominantly expressed on the plasma membrane of glioma cells. These results suggest that FasL expression is common in human astrocytic brain tumors and may cause apoptosis of glioma cells if Fas expression is induced. The frequency of ICE,ICH-1, and CPP32 overexpression appears to correlate with the malignacy grade of astrocytic brain tumors. Furthermore, ICH-1 and CPP32 overexpression may play an important role in the pathogenesis of necrosis, which is one of the histological hallmarks of glioblastoma.
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