| Project/Area Number |
17500220
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Gunma University |
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Principal Investigator |
HIRATO Junko Gunma University, Gumma University Hospital, Department of Pathology, Associate professor (60208832)
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| Co-Investigator(Kenkyū-buntansha) |
神谷 誠 群馬大学, 大学院医学系研究科, 助手 (40344915)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥2,880,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥180,000)
Fiscal Year 2007: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Glioma / Childhood / Myxoid matrix / Histopathology / Immunohistochemistry / Oncogene / 臨床病理学 |
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| Research Abstract |
Ten cases with gliomas with extensive myxoid change were selected from files of brain tumors diagnosed at Gunma University Hospital and cases sent to the author for consultation, and were examined. Patient age of nine cases ranged between 1 and 16 years and 24-old year patient was added. All tumors except a cerebellar tumor arose in supratentorial region. Three cases had developed acute lymphoblastic leukemia(ALL) in their past history.
Tumor tissues showed microcystic change, angiocentric pattern, and sparsely diffuse pattern with extensive myxoid change. Tumor cells appeared to have a tendency of aggregating to perivascular space. The tumors were divided into low-grade and high-grade groups from the aspects of anaplasia and proliferation ability. Five of seven high-grade tumors included small primitive cell component One of them consisted of only small primitive cells that were positive for synaptophysin, and showed high proliferation ability. It was histologically consistent with pri
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mitive neuroectodermal tumor (PNET). In addition to primitive cells, two cases were composed of differentiated astrocytes without anaplasia, and other two cases had diffusely proliferating glioma component showing anaplasia. Two cases without primitive component were similar to high grade astrocytoma, but the tumor cells hardly expressed glial fibrillary acidic protein (GFAP), but did vimentin. Other three cases were classified as low-grade glioma, including pilomyxoid astrocytoma, astrocytic tumor negative for GFAP, and oligodendroglioma-like tumor.
Most myxoid gliomas were high-grade. In addition, they often harbored small primitive cell component Some of them were considered to be a variant of glioblastoma. Small primitive cells frequently expressed Olig2 or 5-100 protein. The finding was different from that of conventional PNET. APNET-like tumor did not overexpress EGFR or p53.
Three cases developed myxoid glioma after remission of ALL by chemotherapy and/or radiotherapy. It is possible that myxoid gliomas may occur as secondary tumor or radiation-induced tumor. Less
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