{"created":"2023-06-20T16:49:18.728876+00:00","id":21505,"links":{},"metadata":{"_buckets":{"deposit":"61424731-74e5-4d3a-ae69-6c4e3dc7c8da"},"_deposit":{"created_by":3,"id":"21505","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"21505"},"status":"published"},"_oai":{"id":"oai:kindai.repo.nii.ac.jp:00021505","sets":["14:2667:4613"]},"author_link":["43217"],"control_number":"21505","item_8_biblio_info_21":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2020","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"5","bibliographicPageStart":"1","bibliographic_titles":[{"bibliographic_title":"科学研究費助成事業研究成果報告書 (2019)"}]}]},"item_8_description_25":{"attribute_name":"リンクURL","attribute_value_mlt":[{"subitem_description":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K15032/","subitem_description_type":"Other"}]},"item_8_description_33":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"研究成果の概要（和文）：本研究には16例のALK-TKIに耐性を獲得したEML4-ALK融合遺伝子陽性肺癌患者を登録。全例で耐性後に血液検体採取し、12例では耐性後に再生検を施行し組織採取ができた。10例で治療前後両方の腫瘍組織検体を集めており、収集した検体から抽出したDNAを用いて行った体細胞遺伝子変異解析から5つの既知のALK遺伝子の2次変異を検出した。2次耐性変異検出例の患者背景としては、男性、非喫煙又は軽喫煙者が多く、全例Alectinibの投与歴を有していた。2次耐性変異検出例では全例で後治療が施行されており、4例で第3世代ALK-TKIであるLorlatinibが投与され、全例で腫瘍縮小効果が得られた。研究成果の概要（英文）：Between November 2016 and May 2019, 16 EML4-ALK fusion gene-positive patients were enrolled following disease progression on first- or second-generation ALK inhibitors. Blood samples were collected in all patients, and re-biopsy was performed in 12 patients. Paired samples of pre- and post-ALK-TKI treatment were collected in 10 patients and next-generation sequencing was performed. Among the 12 patients undergoing ALK-TKI-resistant biopsies, 6 (50.0%) had secondary mutations. The most common ALK resistance mutation was G1202R (2 cases), and the remaining ALK resistance mutations included: G1269A, L1196M, V1180L, and F1174L. The characteristics of patients with secondary mutations were mostly males (83.3%), non-smokers (50%), or light smokers (33.3%), and all patients pretreated with alectinib. Of the 4 patients (66.7%) with secondary mutations were treated with lorlatinib, a third-generation ALK-TKI, and all patients had a response to lorlatinib.","subitem_description_type":"Abstract"}]},"item_8_description_36":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究種目：若手研究(B);  研究期間：2017～2019;   課題番号：17K15032;   研究分野：臨床腫瘍学;   科研費の分科・細目：","subitem_description_type":"Other"}]},"item_8_description_37":{"attribute_name":"資源タイプ(WEKO2)","attribute_value_mlt":[{"subitem_description":"Research Paper","subitem_description_type":"Other"}]},"item_8_description_41":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_description":"application/pdf","subitem_description_type":"Other"}]},"item_8_publisher_14":{"attribute_name":"出版者 名前","attribute_value_mlt":[{"subitem_publisher":"近畿大学"}]},"item_8_text_10":{"attribute_name":"著者 役割","attribute_value_mlt":[{"subitem_text_value":"研究代表者"}]},"item_8_text_7":{"attribute_name":"著者(英)","attribute_value_mlt":[{"subitem_text_language":"en","subitem_text_value":"TANAKA, Kaoru"}]},"item_8_text_8":{"attribute_name":"著者 所属","attribute_value_mlt":[{"subitem_text_value":"近畿大学医学部; 講師"}]},"item_8_text_9":{"attribute_name":"著者所属(翻訳)","attribute_value_mlt":[{"subitem_text_value":"Kindai University"}]},"item_8_version_type_12":{"attribute_name":"版","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_be7fb7dd8ff6fe43","subitem_version_type":"NA"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"田中, 薫"},{"creatorName":"タナカ, カオル","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-03-15"}],"displaytype":"detail","filename":"17K15032seika.pdf","filesize":[{"value":"320.7 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"17K15032seika.pdf","url":"https://kindai.repo.nii.ac.jp/record/21505/files/17K15032seika.pdf"},"version_id":"5ffb7c23-094a-45f3-a638-6a79c6daac26"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"分子標的治療","subitem_subject_scheme":"Other"},{"subitem_subject":"ALK阻害剤","subitem_subject_scheme":"Other"},{"subitem_subject":"薬剤耐性","subitem_subject_scheme":"Other"},{"subitem_subject":"非小細胞肺癌","subitem_subject_scheme":"Other"}]},"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":"ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する研究","subitem_title_language":"ja"},{"subitem_title":"Research on mechanisms of acquired resistance to ALK-TKI in ALK fusion gene positive non-small cell lung cancer","subitem_title_language":"en"}]},"item_type_id":"8","owner":"3","path":["4613"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2021-03-15"},"publish_date":"2021-03-15","publish_status":"0","recid":"21505","relation_version_is_last":true,"title":["ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する研究"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-09-14T05:54:50.022724+00:00"}