{"created":"2023-07-27T06:50:24.655472+00:00","id":43176,"links":{},"metadata":{"_buckets":{"deposit":"84c30e72-6121-4243-b82d-add760ae5201"},"_deposit":{"created_by":18,"id":"43176","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"43176"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00043176","sets":["1777:1778:1779"]},"author_link":["69497","69496","69494","69495"],"item_4_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017-09","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"2017","bibliographicPageEnd":"1731","bibliographicPageStart":"1726","bibliographicVolumeNumber":"108","bibliographic_titles":[{"bibliographic_title":"Cancer Science"}]}]},"item_4_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"北嶋, 俊輔"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"髙橋, 智聡"}],"nameIdentifiers":[{},{}]}]},"item_4_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"The Retinoblastoma (RB) tumor suppressor regulates G1/S transition during cell cycle progression by modulating the activity of E2F transcription factors. The RB pathway plays a central role in the suppression of most cancers, and RB mutation was initially discovered by virtue of its role in tumor initiation. However, as cancer genome sequencing has evolved to profile more advanced and treatment-resistant cancers, it has become increasingly clear that, in the majority of cancers, somatic RB inactivation occurs during tumor progression. Furthermore, despite the presence of deregulation of cell cycle control due to an INK4A deletion, additional CCND amplification and/or other mutations in the RB pathway, mutation or deletion of the RB gene is often observed during cancer progression. Of note, RB inactivation during cancer progression not only facilitates G1/S transition but also enhances some characteristics of malignancy, including altered drug sensitivity and a return to the undifferentiated state. Recently, we reported that RB inactivation enhances pro-inflammatory signaling through stimulation of the interleukin-6/STAT3 pathway, which directly promotes various malignant features of cancer cells. In this review, we highlight the consequences of RB inactivation during cancer progression, and discuss the biological and pathological significance of the interaction between RB and pro-inflammatory signaling. © 2017 Japanese Cancer Association.","subitem_description_type":"Abstract"}]},"item_4_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学がん進展制御研究所  ","subitem_description_type":"Other"}]},"item_4_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00049523","subitem_identifier_reg_type":"JaLC"}]},"item_4_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Japanese Cancer Association / Blackwell Publishing Ltd"}]},"item_4_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1111/cas.13312","subitem_relation_type_select":"DOI"}}]},"item_4_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"http://www.jca.gr.jp/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://www.jca.gr.jp/","subitem_relation_type_select":"URI"}}]},"item_4_rights_23":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"Copyright © 2017 Japanese Cancer Association."}]},"item_4_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AA11808050","subitem_source_identifier_type":"NCID"}]},"item_4_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1347-9032","subitem_source_identifier_type":"ISSN"}]},"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":"Kitajima, Shunsuke"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"Takahashi, Chiaki"}],"nameIdentifiers":[{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-12-22"}],"displaytype":"detail","filename":"CA-PR-TAKAHASHI-C-1726.pdf","filesize":[{"value":"686.4 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-TAKAHASHI-C-1726.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/43176/files/CA-PR-TAKAHASHI-C-1726.pdf"},"version_id":"c9b18365-7784-4d25-86bd-36f3fd0cacc2"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"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":"Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation"}]},"item_type_id":"4","owner":"18","path":["1779"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-12-22"},"publish_date":"2017-12-22","publish_status":"0","recid":"43176","relation_version_is_last":true,"title":["Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T11:06:43.724663+00:00"}