{"created":"2023-07-27T06:53:43.141192+00:00","id":48562,"links":{},"metadata":{"_buckets":{"deposit":"507517fc-cf43-4894-9b18-6f0b473899b6"},"_deposit":{"created_by":18,"id":"48562","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"48562"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00048562","sets":["2812:2813:2815"]},"author_link":["84723","2313"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2019-06-20","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"6p.","bibliographicVolumeNumber":"2015-04-01 - 2019-03-31","bibliographic_titles":[{"bibliographic_title":"平成30(2018)年度 科学研究費補助金 基盤研究(A) 研究成果報告書"},{"bibliographic_title":"2018 Fiscal Year Final Research Report","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":"大腸がん悪性化に関与するドライバー遺伝子の中から異なるパスウェイの制御に関わる５種類（Apc、Kras、Tgfbr2、Trp53、Fbxw7）に着目し、異なる組み合わせで変異を持つマウスモデルを交配により作製して解析した。その結果、Wnt活性化により発生した腸管腫瘍細胞は、TGF-beta経路の遮断または変異p53の発現により粘膜下浸潤し、さらにKrasの活性化変異の蓄積によりEMT様の形態変化と脈管内浸潤が誘導されることを明らかにした。これらの３重遺伝子変異を持つ腫瘍由来オルガノイドは転移能を獲得しており、誘導遺伝子群の中から転移に対する治療標的分子を特定することが期待された。 ","subitem_description_type":"Abstract"},{"subitem_description":"We have selected five colon cancer driver genes, Apc, Kras, Tgfbr2, Trp53 and Fbxw7, which regulate distinct oncogenic or tumor-suppressor pathways, and generated compound mutant mice by intensive crossing. Phenotype analyses of the mice revealed that suppression of TGF-beta signaling or mutant p53 expression in addition to Wnt activation causes submucosal invasion. Moreover, we found that additional Kras activation mutation induces morphological changes to EMT-like structure and intravasation. These triple mutant tumor-derived organoids acquired metastatic ability rom spleen to the liver. Taken together, the results suggest that Apc, Kras, Tgfbr2 or Apc, Kras, Trp53 is a minimum core for efficient colon cancer metastasis. ","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:15H02362, 研究期間(年度):2015-04-01 - 2019-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「大腸がん自然転移・再発モデルの開発による悪性化進展機構の研究」課題番号15H02362\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-15H02362/15H02362seika/）を加工して作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00054884","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学新学術創成研究機構ナノ生命科学研究所"}]},"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=40324610"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=40324610","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15H02362/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15H02362/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15H02362/15H02362seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15H02362/15H02362seika/","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":"2020-04-27"}],"displaytype":"detail","filename":"CA-PR-OSHIMA-M-kaken 2019-6p.pdf","filesize":[{"value":"404.0 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-OSHIMA-M-kaken 2019-6p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/48562/files/CA-PR-OSHIMA-M-kaken 2019-6p.pdf"},"version_id":"dc5f521c-c4e7-4dd9-aa35-c524e52fd23b"}]},"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":"大腸がん自然転移・再発モデルの開発による悪性化進展機構の研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"大腸がん自然転移・再発モデルの開発による悪性化進展機構の研究"},{"subitem_title":"Analysis on colon cancer malignant progression using novel mouse models","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2815"],"pubdate":{"attribute_name":"公開日","attribute_value":"2020-04-27"},"publish_date":"2020-04-27","publish_status":"0","recid":"48562","relation_version_is_last":true,"title":["大腸がん自然転移・再発モデルの開発による悪性化進展機構の研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:33:46.271419+00:00"}