{"created":"2023-07-27T06:55:16.654018+00:00","id":51055,"links":{},"metadata":{"_buckets":{"deposit":"61c43260-58b4-4c4c-a22f-e1c1f0f471c4"},"_deposit":{"created_by":18,"id":"51055","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"51055"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00051055","sets":["2812:2813:2835"]},"author_link":["21834","92452"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"1999-12-07","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"2p.","bibliographicVolumeNumber":"1997-1998","bibliographic_titles":[{"bibliographic_title":"平成10(1998)年度 科学研究費補助金 基盤研究(B) 研究成果報告書概要"},{"bibliographic_title":"1998 Fiscal Year Final Research Report Summary","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Cysteine proteases of caspase family (interleukin-1 beta -converting enzyme) 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 of Caspase-1, Caspase-2 and Caspase-3 in 11 cases of primary astrocytic tumors ( five anaplastic astrocytomas, and six glioblastomas) by reverse transcription (RT)-PCR, Western blot analysis, immunohistochemistry, and in situ casspase-3 activity assay. The frequency of Caspase-1, Caspase-2 and Caspase-3 overexpression appears to correlate with the malignancy grade of astrocytic brain tumors. Furthermore, Caspase-2 and Caspase-3 overexpression and Caspase-3 activation may play an important role in the pathogenesis of necrosis, which is one of the histological hallmarks of glioblastoma.","subitem_description_type":"Abstract"},{"subitem_description":"神経膠芽腫が摘出時多数の壊死巣が認められるという脳腫瘍病理学上の基本問題を分子生物学的に解明し、この機序を利用して治療に結び付けることをことを目指しており、壊死発現機構を壊死誘発因子と壊死原因遺伝子の解析をおこなった。\n(1)悪性神経膠腫の細胞株U87MG.T98Gに対して、生体内に極めて近い状態で壊死誘発因子となりうるもの、すなわち1)低酸素、2)低栄養状態の刺激を加えて細胞死の誘発が可能かどうかを調べた。この結果72時間の刺激では細胞死を誘発することができなかった。変わって抗癌剤では腫瘍細胞死を誘発することができた。抗癌剤の刺激のためかFas/Fas-ligand経路は腫瘍細胞死には関与しなかった。カスパーゼの中ではCaspase-3のみが抗癌剤による細胞死に関与し、U87MGおよびT98Gに対するCDDP刺激でpro-Caspase-3の増加と活性化が36時間後に得られ、24時間後からPARPの切断化が出現しアポトーシスが誘発された。(2)ヒト神経膠芽腫摘出材料11例に対して、壊死周辺細胞におけるFas,Fas-L,Casp-1.2.3の抗体で同定した。その結果、壊死巣周辺のみの腫瘍細胞に有意に発現していたものはFasとCaspase-3であった。さらに、Casepase-3の活性型をin situで同定した。このことから、壊死巣周辺では何らかの刺激に対してFasとCaspase.3の過剰発現さらに活性化が生じアボトーシスが誘発されることが示唆された。以上より、神経膠芽腫の壊死誘発遺伝子の最終経路として、Casepase-3の活性化が重要であり、今後はCasepase-3の活性化を誘発する治療の開発に取り組む予定である。","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:09470292, 研究期間(年度):1997-1998","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「悪性神経膠腫における壊死原因遺伝子の解析」課題番号09470292\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） \n（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-09470292/094702921998kenkyu_seika_hokoku_gaiyo/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学医薬保健研究域医学系","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00057358","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=90026948"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=90026948","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09470292/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09470292/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-09470292/094702921998kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-09470292/094702921998kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2022-05-20"}],"displaytype":"detail","filename":"ME-PR-YAMASHITA-J-kaken 1999-2p.pdf","filesize":[{"value":"81.7 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-YAMASHITA-J-kaken 1999-2p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/51055/files/ME-PR-YAMASHITA-J-kaken 1999-2p.pdf"},"version_id":"2103dd97-af43-4cb6-b9a7-883d54dba8d5"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"悪性神経膠腫における壊死原因遺伝子の解析","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"悪性神経膠腫における壊死原因遺伝子の解析"},{"subitem_title":"Analysis of cell death inducing gene in human malignant gliomas","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2835"],"pubdate":{"attribute_name":"公開日","attribute_value":"2022-05-20"},"publish_date":"2022-05-20","publish_status":"0","recid":"51055","relation_version_is_last":true,"title":["悪性神経膠腫における壊死原因遺伝子の解析"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:04:38.529965+00:00"}