{"created":"2023-07-27T06:53:25.804444+00:00","id":48103,"links":{},"metadata":{"_buckets":{"deposit":"a56dddd0-975a-43e8-b31e-2efaa0b91ab7"},"_deposit":{"created_by":18,"id":"48103","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"48103"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00048103","sets":["2812:2813:2815"]},"author_link":["227","71948"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2019-06-19","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"5p.","bibliographicVolumeNumber":"2016-04-01 - 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(C) 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":"本研究では、胃がんの悪性化機構を個体レベルで明らかにすることを目的とし、新規マウスモデルの開発と解析を推進した。胃炎を伴う胃粘膜上皮特異的に発現するClaudin2と、正常胃粘膜上皮で持続的に発現するClaudin18遺伝子のプロモーター領域でCreERを発現するマウスの樹立に成功した。これらのマウスを、胃がん発症マウスと胃がん悪性化への関与が指摘されるTgfbr2およびTrp53遺伝子変異マウスとの交配を行ない、胃病変の病理解析の結果、TGF-betaシグナル遮断や変異型p53発現はどちらも悪性化を誘導せず、胃がん悪性化にはさらに遺伝子変異の蓄積が必要と考えられた。 ","subitem_description_type":"Abstract"},{"subitem_description":"In this project, we tried to establish a new mouse model for gastric cancer with metastasis using Gan mice together with conditional gene knockout mice. First we constructed CreER expressing mice in the gastric mucosa using Claudin2 and Claudin18 promoter. Claudin2 expresses in the inflamed gastric epitherial cells and Claudin18 expresses in the normal gastric epithelia. Then, we crossed Gan mice that develop gastric tumors and Tgfbr2 conditional KO mice or p53 conditional KO mice together with Cldn18-CreERT2 mice. And these mice were treated with Tamoxifen. However, disruption of Tgfbr2 gene and additional p53 gene mutation did not cause any morphological changes or invasion phenotype of gastric tumors of Gan mice. These results indicate that TGF beta signaling and p53 mutation are not sufficient for gastric tumor malignant progression. ","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:16K07111, 研究期間(年度):2016-04-01 - 2019-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「新規胃がんモデルの開発による悪性化進展機構の研究」課題番号16K07111\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-16K07111/16K07111seika/）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":"10.24517/00054425","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学がん進展制御研究所"}]},"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=80362515"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=80362515","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K07111/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K07111/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16K07111/16K07111seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16K07111/16K07111seika/","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":"2020-04-23"}],"displaytype":"detail","filename":"CA-PR-OSHIMA-H-kaken 2019-5p.pdf","filesize":[{"value":"472.4 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-OSHIMA-H-kaken 2019-5p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/48103/files/CA-PR-OSHIMA-H-kaken 2019-5p.pdf"},"version_id":"12750308-20ea-4811-b6f0-7d46e216ecba"}]},"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":"新規胃がん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":"新規胃がんモデルの開発による悪性化進展機構の研究"},{"subitem_title":"Establishment of novel gastric cancer mouse models","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2815"],"pubdate":{"attribute_name":"公開日","attribute_value":"2020-04-23"},"publish_date":"2020-04-23","publish_status":"0","recid":"48103","relation_version_is_last":true,"title":["新規胃がん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":"2023-07-27T13:37:02.776671+00:00"}