{"created":"2023-07-27T06:28:50.782184+00:00","id":13417,"links":{},"metadata":{"_buckets":{"deposit":"4cd842d8-8d39-4e69-9a17-4d4518449833"},"_deposit":{"created_by":3,"id":"13417","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"13417"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00013417","sets":["1132:1133:1134"]},"author_link":["20454","97"],"item_4_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2011-08-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"8","bibliographicPageEnd":"1255","bibliographicPageStart":"1253","bibliographicVolumeNumber":"24","bibliographic_titles":[{"bibliographic_title":"泌尿器外科 = Japanese journal of urological surgery"}]}]},"item_4_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"去勢抵抗性前立腺癌への移行には様々な機序が関与していると考えられている. アンドロゲン受容体(AR)を介さない経路ARを介してもアンドロゲンを介さない経路, AR mutation, 癌細胞のアンドロゲン高感受性への変化, 前立腺癌組織内での副腎性アンドロゲンからのDHT生合成などに大きく分けられる. 多くの場合, アンドロゲンとアンドロゲン受容体が関与していると考えられる. 「はじめに」前立腺癌は, リンパ節や骨に転移があっても去勢術によりほとんどの症例で症状やPSA値の改善が認められる. 多くの前立腺癌ではアンドロゲン受容体(以下, AR)が発現して, アンドロゲンが増殖因子として癌の進行に多大な影響を与えているためである. また, 再燃時(以下, CRPC)にも, ARが何らかの働きをして再燃が引き起こされていると考えられる. このCRPCの原因について, ARを中心に述べたい. 1. ARを介さない経路 1)AR発現の消失 ARプロモータ領域のDNAのメチレーションのほか, 発現に重要な転写因子が何らかの原因でプロモータに作用しなかったり, 5'-UTRに結合する翻訳因子がうまく働かなければ, ARの発現は消失か減弱する.","subitem_description_type":"Abstract"}]},"item_4_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"医学図書出版"}]},"item_4_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://www.igakutosho.co.jp/","subitem_relation_type_select":"URI"}}]},"item_4_rights_23":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"Copyright © 医学図書出版 | 許可を得て登録"}]},"item_4_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AN10064459","subitem_source_identifier_type":"NCID"}]},"item_4_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0914-6180","subitem_source_identifier_type":"ISSN"}]},"item_4_text_2":{"attribute_name":"その他のタイトル","attribute_value_mlt":[{"subitem_text_value":"1. CRPCの基礎的原因"},{"subitem_text_value":"[第26回前立腺シンポジウム記録]基礎部門セッション4不応性機序"},{"subitem_text_value":"Mechanisms of transition into castration-resistant prostate cancer"}]},"item_4_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"溝上, 敦"}],"nameIdentifiers":[{},{},{},{}]},{"creatorNames":[{"creatorName":"並木, 幹夫"}],"nameIdentifiers":[{},{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-03"}],"displaytype":"detail","filename":"ME-PR-MIZOKAMI-A-1253.pdf","filesize":[{"value":"2.6 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"ME-PR-MIZOKAMI-A-1253.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/13417/files/ME-PR-MIZOKAMI-A-1253.pdf"},"version_id":"97bd60cf-2052-488f-b26d-ccccfcdbba12"}]},"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":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"CRPCの基礎的原因","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"CRPCの基礎的原因"}]},"item_type_id":"4","owner":"3","path":["1134"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-03"},"publish_date":"2017-10-03","publish_status":"0","recid":"13417","relation_version_is_last":true,"title":["CRPCの基礎的原因"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-07-28T01:05:27.252003+00:00"}