{"created":"2023-07-27T06:58:40.114165+00:00","id":57555,"links":{},"metadata":{"_buckets":{"deposit":"ae95b4d2-3c01-41a7-abda-f71dfcae64db"},"_deposit":{"created_by":18,"id":"57555","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"57555"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00057555","sets":["2812:2813:2832"]},"author_link":["100603","21832"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2003-09-16","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"2p.","bibliographicVolumeNumber":"2000 – 2001","bibliographic_titles":[{"bibliographic_title":"平成13(2001)年度 科学研究費補助金 基盤研究(C) 研究概要"},{"bibliographic_title":"2001 Research Project 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":"神経膠芽腫は外科的全摘出が不可能で、残存腫瘍に対する効果的治療がない。一方、本腫瘍の病理学上の特徴である壊死巣の原因は十分解明されておらず、壊死巣の形成機構が同定できればこれを利用した治療の開発に結び付く。ヒト神経膠芽腫の細胞死に結び付く遺伝子としてFas/AP01(CD95)の発現と壊死細胞との関係を報告し、Fas-ligand(FasL)のヒト神経膠芽腫における発現も見いだした。しかし、なぜFasとFasLが同時に発現するのかは不明である。FasLと強い親和性を示すdecoy receptor 3(DcR3)に注目し、Fas、FasLおよびDcR3の遺伝子発現および蛋白の過剰発現を神経膠腫の症例に対して解析を行った。\nPcR3遺伝子の増幅の有無を半定量的PCR法を用い、DcR 3mRNAの発現をリアルタイム半定量的逆転写一PCR法にて、Fas蛋白及びFasL蛋白の発現を免疫組織化学法を用いてそれぞれ検討した。手術標本より得られた57例の星細胞系神経膠腫を対象とした。DcR3遺伝子増幅を星細胞腫(7例)では1例も認めず、退形成星細胞腫では16例中の1例に、神経膠芽腫では34例中の7例に認めた。DcR3mRNAの発現は、神経膠芽腫群でより高い傾向にあった。DcR3のDNAコピー数の異常とmRNA発現量との間には統計学的相関関係を認めた(p=0.02)。Fas蛋白は星細胞腫群では陽性反応を呈するものは1例も認めなかったが、退形成星細胞腫では16例中3例に、神経膠芽腫では34例中21例において腫瘍細胞に発現を認めた。FasL蛋白は星細胞腫7例中3例に、退形成星細胞腫16例中9例に、神経膠芽腫では34例中29例において腫瘍細胞に発現を認めた。以上より、DcR3は星細胞系神経膠腫の悪性化において重要な役割を果たしていることが示唆された。また、DcR3はFasやFasLに陽性を示す神経膠芽腫群で多く発現することから、Fas/FasL依存性の細胞死を回避する機能を有する可能性が推察された。","subitem_description_type":"Abstract"},{"subitem_description":"Decoy receptor 3 (DcR3), a secreted member of the tumor necrosis factor receptor superfamily, is amplified at high frequency in human lung and colon. In this study, I examined the DcR3 gene amplification by semi-quantitative genomic PCR in 57 human astrocytic brain tumors, including 34 glioblastomas and DcR3 mRNA expression by real-time semi-quantitative reverse transcription-PCR in 24 astrocytic brain tumors, including 13 glioblastomas. DcR3 gene amplification was detected in none of 7 (0%) low-grade astrocytomas, 1 of 17 (5.9%) anaplastic astrocytomas, and 7 of 34 (20.6%) glioblastomas. DcR3 mRNA tend to express high in glioblastomas than low grade astrocytomas. A well correlation between DcR3 gene amplification and mRNA expression was found in 24 astrocytic tumors. Expression of DcR3 mRNA in human astrocytic tumors was dependent of gene amplification. Immunoreactivity to Fas was observed in a large number of glioblastoma cases. These results suggest that high DcR3 expression with gene amplification might be responsible to malignant featuresin high grade astrocytic tumors, that may be attributed to escape from FasL-Fas mediated cell death.","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:12671346, 研究期間(年度):2000 – 2001","subitem_description_type":"Other"},{"subitem_description":"出典：「ヒト神経膠芽腫における壊死巣形成機構を標的とした治療の基礎的研究」研究成果報告書　課題番号12671346\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/grant/KAKENHI-PROJECT-12671346/）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・附属病院","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00063825","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-12671346/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-12671346/","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":"2021-09-03"}],"displaytype":"detail","filename":"HO-PR-TACHIBANA-O-kaken 2003-2p.pdf","filesize":[{"value":"68.7 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"HO-PR-TACHIBANA-O-kaken 2003-2p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/57555/files/HO-PR-TACHIBANA-O-kaken 2003-2p.pdf"},"version_id":"171210f1-54ae-4476-a0e8-84a0c592d8e0"}]},"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":"ヒト神経膠芽腫における壊死巣形成機構を標的とした治療の基礎的研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"ヒト神経膠芽腫における壊死巣形成機構を標的とした治療の基礎的研究"},{"subitem_title":"Necrogenesis in human astrocytic tumors especially based on decoy receptor 3 gene amplification and expression","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2832"],"pubdate":{"attribute_name":"公開日","attribute_value":"2021-09-03"},"publish_date":"2021-09-03","publish_status":"0","recid":"57555","relation_version_is_last":true,"title":["ヒト神経膠芽腫における壊死巣形成機構を標的とした治療の基礎的研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T14:57:12.357582+00:00"}