{"_buckets": {"deposit": "83ff566e-f11b-4981-a51e-852909028000"}, "_deposit": {"id": "14804", "owners": [], "pid": {"revision_id": 0, "type": "depid", "value": "14804"}, "status": "published"}, "_oai": {"id": "oai:nagoya.repo.nii.ac.jp:00014804", "sets": ["1403"]}, "item_9_biblio_info_6": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2012-08", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "3-4", "bibliographicPageEnd": "271", "bibliographicPageStart": "261", "bibliographicVolumeNumber": "74", "bibliographic_titles": [{"bibliographic_title": "Nagoya Journal of Medical Science"}]}]}, "item_9_description_4": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "Cytokine-dependent cell lines have been used to analyze the cytokine-induced cellular signaling and the mechanism of oncogenesis. In the current study, we analyzed MOTN-1 and PLT-2 cell lines established from different stages of a T-cell large granular lymphocyte leukemia patient (Daibata et al. 2004). MOTN-1 is IL-2-dependent derived from the chronic phase, whereas IL-2-independent PLT-2 is from the aggressive and terminal stage. They shared considerable chromosome abnormalities and the pattern of T-cell receptor rearrangement, presuming that the cytokine independence of PLT-2 was due to the additive genetic abnormality. Besides IL-2, IL-15 supported MOTN-1 cell growth, because these receptors share b- and g-subunits. IL-2 activated ERK, AKT and STAT pathway of MOTN-1. STAT3 pathway of PLT-2 was also activated by IL-2, suggesting intact IL-2 induces signal transduction of PLT-2. However, ERK1/2 but not AKT, was continuously activated in PLT-2, consistent with the increased Ras-activity of PLT-2. Sequence analysis revealed KRAS G12A mutation but not NRAS and HRAS mutation of PLT-2 but not MOTN-1. Another signaling molecule affecting Ras-signaling pathway, SHP2, which has been frequently mutated in juvenile myelomonocytic leukemia (JMML), did not show mutation. Moreover, MEK inhibitor, PD98059, as well as farnesylation inhibitor inhibited PLT-2 cell growth. Using NIH3T3 and MOTN-1, ERK activation, increased cell proliferation and survival by KRAS G12A were shown, suggesting the important role of KRAS G12A in IL-2-independent growth of PLT-2. Taken together, KRAS G12A is important for IL-2-independent growth of PLT-2 cells and suggests the possibility of involvement of KRAS mutation with disease progression.", "subitem_description_type": "Abstract"}]}, "item_9_identifier_60": {"attribute_name": "URI", "attribute_value_mlt": [{"subitem_identifier_type": "URI", "subitem_identifier_uri": "http://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/7434/7434.html"}, {"subitem_identifier_type": "HDL", "subitem_identifier_uri": "http://hdl.handle.net/2237/16737"}]}, "item_9_identifier_registration": {"attribute_name": "ID登録", "attribute_value_mlt": [{"subitem_identifier_reg_text": "10.18999/nagjms.74.3-4.261", "subitem_identifier_reg_type": "JaLC"}]}, "item_9_publisher_32": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "Nagoya University School of Medicine"}]}, "item_9_select_15": {"attribute_name": "著者版フラグ", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_9_source_id_7": {"attribute_name": "ISSN（print）", "attribute_value_mlt": [{"subitem_source_identifier": "0027-7622", "subitem_source_identifier_type": "ISSN"}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "MIZUTANI, NAOKI"}], "nameIdentifiers": [{"nameIdentifier": "45739", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "ITO, HIROMI"}], "nameIdentifiers": [{"nameIdentifier": "45740", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "HAGIWARA, KAZUMI"}], "nameIdentifiers": [{"nameIdentifier": "45741", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "KOBAYASHI, MISA"}], "nameIdentifiers": [{"nameIdentifier": "45742", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "HOSHIKAWA, ASUKA"}], "nameIdentifiers": [{"nameIdentifier": "45743", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "NISHIDA, YAYOI"}], "nameIdentifiers": [{"nameIdentifier": "45744", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "TAKAGI, AKIRA"}], "nameIdentifiers": [{"nameIdentifier": "45745", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "KOJIMA, TETSUHITO"}], "nameIdentifiers": [{"nameIdentifier": "45746", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "SUZUKI, MOTOSHI"}], "nameIdentifiers": [{"nameIdentifier": "45747", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "OSAWA, YOSUKE"}], "nameIdentifiers": [{"nameIdentifier": "45748", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "OHNISHI, KAZUNORI"}], "nameIdentifiers": [{"nameIdentifier": "45749", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "DAIBATA, MASANORI"}], "nameIdentifiers": [{"nameIdentifier": "45750", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "MURATE, TAKASHI"}], "nameIdentifiers": [{"nameIdentifier": "45751", "nameIdentifierScheme": "WEKO"}]}]}, "item_files": {"attribute_name": "ファイル情報", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2018-02-20"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "05_Mizutani.pdf", "filesize": [{"value": "489.1 kB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_free", "mimetype": "application/pdf", "size": 489100.0, "url": {"label": "05_Mizutani.pdf", "url": "https://nagoya.repo.nii.ac.jp/record/14804/files/05_Mizutani.pdf"}, "version_id": "b346ee80-5fa3-4925-beea-e44054908f12"}]}, "item_keyword": {"attribute_name": "キーワード", "attribute_value_mlt": [{"subitem_subject": "Human LGL leukemia cell lines", "subitem_subject_scheme": "Other"}, {"subitem_subject": "MOTN-1 and PLT-2", "subitem_subject_scheme": "Other"}, {"subitem_subject": "IL-2 independent growth", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Ras/MAP/ERK pathway", "subitem_subject_scheme": "Other"}, {"subitem_subject": "KRAS G12A mutation", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Ras activity", "subitem_subject_scheme": "Other"}]}, "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": "departmental bulletin paper", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_title": "INVOLVEMENT OF KRAS G12A MUTATION IN THE IL-2-INDEPENDENT GROWTH OF A HUMAN T-LGL LEUKEMIA CELL LINE, PLT-2", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "INVOLVEMENT OF KRAS G12A MUTATION IN THE IL-2-INDEPENDENT GROWTH OF A HUMAN T-LGL LEUKEMIA CELL LINE, PLT-2"}]}, "item_type_id": "9", "owner": "1", "path": ["1403"], "permalink_uri": "https://doi.org/10.18999/nagjms.74.3-4.261", "pubdate": {"attribute_name": "公開日", "attribute_value": "2012-08-29"}, "publish_date": "2012-08-29", "publish_status": "0", "recid": "14804", "relation": {}, "relation_version_is_last": true, "title": ["INVOLVEMENT OF KRAS G12A MUTATION IN THE IL-2-INDEPENDENT GROWTH OF A HUMAN T-LGL LEUKEMIA CELL LINE, PLT-2"], "weko_shared_id": null}