{"created":"2023-07-27T06:58:05.890736+00:00","id":55729,"links":{},"metadata":{"_buckets":{"deposit":"11d92b62-f38e-4515-bc30-0285bfb1c1e3"},"_deposit":{"created_by":18,"id":"55729","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"55729"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00055729","sets":["2812:2813:2819"]},"author_link":["97907"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2015-06-08","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"4p.","bibliographicVolumeNumber":"2013 – 2014","bibliographic_titles":[{"bibliographic_title":"平成26(2014)年度 科学研究費補助金 若手研究(B) 研究成果報告書"},{"bibliographic_title":"2014 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":[{"creatorName":"Naito, Hisamichi"}],"nameIdentifiers":[{"nameIdentifier":"97907","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"30570676","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=30570676"}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"腫瘍の増大には血管新生が必須である。これまでに増殖能が非常に高い幹・前駆細胞様の性質を持った血管内皮細胞が全身の血管に存在する事を明らかにした。血管新生時にはこの特殊な内皮細胞が血管を構築する内皮細胞を大量に産生する。本研究では腫瘍血管で、このような幹・前駆細胞様の内皮細胞の解析を行った。腫瘍血管においては増殖能の高い内皮細胞は正常組織よりも高頻度で認めること、さらに正常組織とは異なる表面マーカーを持つことが明らかになった。また、この内皮細胞と腫瘍をマウス皮下に共移植するとこの内皮細胞由来の腫瘍血管が構築された。この細胞を特異的に阻害することにより、効果的な血管新生阻害剤が開発できる。","subitem_description_type":"Abstract"},{"subitem_description":"Angiogenesis is regarded as a hallmark in cancer development.In the previous work, we identified stem/progenitor like endothelial cell(EC) in the peripheral blood vessel. These endothelial stem-like cell possess EC colony-forming potential in vitro and contribute to angiogenesis by generating functional mature blood vessels in vivo. In this study, we characterized endothelial stem-like cells in the tumor vasculature and found that in the tumor vasclature, the percentage of stem-like cells were higher than normal tissues. We further examined contribution of these cells to the tumor vasculature by transplantation model and found that they produces numbers of ECs and contribute to the tumor blood vessels as functional vessels. Moreover, administration of anti-angiogenic drugs revealed their potential role for resistance to anti-angiogenic therapy.","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:25830080, 研究期間(年度):2013 - 2014","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「腫瘍血管内皮幹細胞制御による新規血管新生阻害療法の開発」課題番号25830080\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-25830080/25830080seika/）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":"金沢大学医薬保健研究域医学系 / 大阪大学","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00062004","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/search/?qm=30570676"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=30570676","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-25830080/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-25830080/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-25830080/25830080seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-25830080/25830080seika/","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_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"内藤, 尚道"}],"nameIdentifiers":[{"nameIdentifier":"97907","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"30570676","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=30570676"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-06-04"}],"displaytype":"detail","filename":"ME-PR-NAITO-H-kaken 2015-4p.pdf","filesize":[{"value":"243.8 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-NAITO-H-kaken 2015-4p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/55729/files/ME-PR-NAITO-H-kaken 2015-4p.pdf"},"version_id":"0feceb26-f58e-4ae8-9437-a2893b3c2369"}]},"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":"腫瘍血管内皮幹細胞制御による新規血管新生阻害療法の開発","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"腫瘍血管内皮幹細胞制御による新規血管新生阻害療法の開発"},{"subitem_title":"Characterization of endothelial side population cells in the tumor vasculature and their potential role for drug resistance.","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2819"],"pubdate":{"attribute_name":"公開日","attribute_value":"2021-06-04"},"publish_date":"2021-06-04","publish_status":"0","recid":"55729","relation_version_is_last":true,"title":["腫瘍血管内皮幹細胞制御による新規血管新生阻害療法の開発"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2024-07-01T05:48:23.270910+00:00"}