{"created":"2023-07-27T06:58:45.029976+00:00","id":57762,"links":{},"metadata":{"_buckets":{"deposit":"22d66d6f-e907-4a4f-8bd8-05e80d826cd7"},"_deposit":{"created_by":18,"id":"57762","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"57762"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00057762","sets":["2812:2813:2834"]},"author_link":["100603","21832"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2001-10-22","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"2p.","bibliographicVolumeNumber":"1998 – 1999","bibliographic_titles":[{"bibliographic_title":"平成11(1999)年度 科学研究費補助金 基盤研究(C) 研究成果報告書概要"},{"bibliographic_title":"1999 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":"神経膠芽腫の壊死巣は大壊死巣(large necrosis)と小壊死巣(pseudopallisading)に分類される。本腫瘍における異なる壊死巣の機序が同定できれば、これを利用した治療の開発に結び付く可能性が考えられる。2種類の壊死巣形成機構とdeath receptor/death ligandの解析により、この機序を利用して治療に結び付けることを目指し、壊死原因遺伝子の解析をおこなった。\n神経膠芽腫の手術摘出材料10例において、小壊死巣と大壊死巣をそれぞれ認める5例づつを選び、壊死誘発遺伝子発現細胞の局在をTUNEL法、免役組織化学療法を用いて検討した。あわせて、RT-PCR法を用いて、TRAIL、DR4、DR5、DcR2、DcR3のmRNAの発現を検討した。抗体はFADD、Fas-L、TRAIL、DR4、DR5、DcR1、DcR1、DcR2、プロカスパーゼ3、活性型カスパーゼ3、プロカスパーゼ9、チトクロームCおよびPARPに対する抗体を使用した。結果はFADD、Fas-L、TRAIL、チトクロームCおよびPARPが全症例において、壊死巣とは関係なく大部分の腫瘍細胞に発現がみられた。DR4は血管内皮細胞に発現がみられた。DcR1、DcR2、プロカスパーゼ9は一部の症例で腫瘍細胞に発現がみられた。DR5は大壊死巣の周囲の腫瘍細胞に発現がみられ、プロカスパーゼ3および活性型カスパーゼ3は小壊死巣の周囲の細胞に発現がみられTUNEL陽性のアポトーシスをきたした細胞と使い関係を示した。DR5とTRAIL発現細胞の局在は、FasとFas-Lの局在の関係と極めて類似していた。小壊死巣におけるカスパーゼ3、特に活性型の発現は、本形態学特徴と極めて強い関係を示した。以上より、神経膠芽腫の組織学特徴である小壊死巣と大壊死巣は、異なった機構により発生すると考えられた。すなわち、大壊死巣は周囲の腫瘍細胞がdeath receptroであるFas、DR5を発現しており、小壊死巣はカスパーゼ3の活性により特徴づけられるものと考えられた。","subitem_description_type":"Abstract"},{"subitem_description":"In the present study, I assesed the expression of death receptor, including Fas/APO-1 (CD95), DR4, and DR5, death ligand (Fas ligand, TRAIL), and decoy receptor, and its relation to necrosis phenotype in glioblastomas. I previously reported that Fas expression is predominantly induced in perinecrotic glioma cells, suggesting that Fas induction is associated with apoptosis and necrosis formation, a histological hallmark of glioblastomas. In this study, DR5 expression is induced in large necrosis, like Fas expression. Fas L and TRAIL were expressed in glioblastoma cells. Caspase-3 overexpression and activated appears to correlate with small necrosis area. These results suggested that necrosis phenotype in glioblastoma were different cell death pathway, and small necrosis was dependent to caspase-3 activation and large necrosis dependent to death receptors.","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:10671288, 研究期間(年度):1998 – 1999","subitem_description_type":"Other"},{"subitem_description":"出典：「ヒト悪性神経膠腫における壊死誘発遺伝子標的治療の基礎的研究」研究成果報告書　課題番号10671288\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/ja/report/KAKENHI-PROJECT-10671288/106712881999kenkyu_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":"金沢大学医学部","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00064032","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/ja/search/?kw=40211362"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/search/?kw=40211362","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-10671288/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-10671288/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-10671288/106712881999kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-10671288/106712881999kenkyu_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":"2021-09-06"}],"displaytype":"detail","filename":"ME-PR-TACHIBANA-O-kaken 2001-2p.pdf","filesize":[{"value":"74.9 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-TACHIBANA-O-kaken 2001-2p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/57762/files/ME-PR-TACHIBANA-O-kaken 2001-2p.pdf"},"version_id":"a7e04504-7c69-4661-93a3-d93f3ab47f16"}]},"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":"ヒト悪性神経膠腫における壊死誘発遺伝子標的治療の基礎的研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"ヒト悪性神経膠腫における壊死誘発遺伝子標的治療の基礎的研究"},{"subitem_title":"Expression of death receptor and death ligand in human astrocytic brain tumors","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2834"],"pubdate":{"attribute_name":"公開日","attribute_value":"2021-09-06"},"publish_date":"2021-09-06","publish_status":"0","recid":"57762","relation_version_is_last":true,"title":["ヒト悪性神経膠腫における壊死誘発遺伝子標的治療の基礎的研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T14:55:27.280901+00:00"}