{"created":"2024-12-03T03:08:33.475262+00:00","id":2002088,"links":{},"metadata":{"_buckets":{"deposit":"d4921bb5-6364-4efc-865a-2cd8ce6bec75"},"_deposit":{"created_by":8,"id":"2002088","owners":[8],"pid":{"revision_id":0,"type":"depid","value":"2002088"},"status":"published"},"_oai":{"id":"oai:fmu.repo.nii.ac.jp:02002088","sets":["1732778801467:1732778962699:1733193809282"]},"author_link":[],"item_1617186331708":{"attribute_name":"Title","attribute_value_mlt":[{"subitem_title":"Cellular carcinogenesis in preleukemic conditions: drivers and defenses","subitem_title_language":"en"}]},"item_1617186419668":{"attribute_name":"Creator","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Ueda, Koki","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Ikeda, Kazuhiko","creatorNameLang":"en"}]}]},"item_1617186499011":{"attribute_name":"Rights","attribute_value_mlt":[{"subitem_rights":"© 2024 The Fukushima Society of Medical Science. This article is licensed under a Creative Commons [Attribution-NonCommercial-ShareAlike 4.0 International] license.","subitem_rights_language":"en","subitem_rights_resource":"https://creativecommons.org/licenses/by-nc-sa/4.0/"}]},"item_1617186609386":{"attribute_name":"Subject","attribute_value_mlt":[{"subitem_subject":"acute myeloid leukemia","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"HMGA2","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"leukemia stem cell","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"MDMX","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"myeloproliferative neoplasms","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"preleukemia","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"Mice","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Humans","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Animals","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Preleukemia","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Tumor Suppressor Protein p53","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Leukemia, Myeloid, Acute","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Hematopoietic Stem Cells","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Mutation","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"},{"subitem_subject":"Cell Transformation, Neoplastic","subitem_subject_language":"en","subitem_subject_scheme":"MeSH"}]},"item_1617186626617":{"attribute_name":"Description","attribute_value_mlt":[{"subitem_description":"Acute myeloid leukemia (AML) arises from preleukemic conditions. We have investigated the pathogenesis of typical preleukemia, myeloproliferative neoplasms, and clonal hematopoiesis. Hematopoietic stem cells in both preleukemic conditions harbor recurrent driver mutations; additional mutation provokes further malignant transformation, leading to AML onset. Although genetic alterations are defined as the main cause of malignant transformation, non-genetic factors are also involved in disease progression. In this review, we focus on a non-histone chromatin protein, high mobility group AT-hook2 (HMGA2), and a physiological p53 inhibitor, murine double minute X (MDMX). HMGA2 is mainly overexpressed by dysregulation of microRNAs or mutations in polycomb components, and provokes expansion of preleukemic clones through stem cell signature disruption. MDMX is overexpressed by altered splicing balance in myeloid malignancies. MDMX induces leukemic transformation from preleukemia via suppression of p53 and p53-independent activation of WNT/β-catenin signaling. We also discuss how these non-genetic factors can be targeted for leukemia prevention therapy.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_1617186643794":{"attribute_name":"Publisher","attribute_value_mlt":[{"subitem_publisher":"The Fukushima Society of Medical Science","subitem_publisher_language":"en"}]},"item_1617186702042":{"attribute_name":"Language","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_1617186920753":{"attribute_name":"Source Identifier","attribute_value_mlt":[{"subitem_source_identifier":"0016-2590","subitem_source_identifier_type":"PISSN"},{"subitem_source_identifier":"2185-4610","subitem_source_identifier_type":"EISSN"},{"subitem_source_identifier":"AA0065246X","subitem_source_identifier_type":"NCID"}]},"item_1617187056579":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2024","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"24","bibliographicPageStart":"11","bibliographicVolumeNumber":"70","bibliographic_titles":[{"bibliographic_title":"Fukushima Journal of Medical Science","bibliographic_titleLang":"en"}]}]},"item_1617258105262":{"attribute_name":"Resource Type","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_1617265215918":{"attribute_name":"Version Type","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_1617353299429":{"attribute_name":"Relation","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"https://doi.org/10.5387/fms.2023-17","subitem_relation_type_select":"DOI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"37952978","subitem_relation_type_select":"PMID"}}]},"item_1617605131499":{"attribute_name":"File","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_access","date":[{"dateType":"Available","dateValue":"2024-02-01"}],"displaytype":"detail","filename":"FksmJMedSci_70_p11.pdf","filesize":[{"value":"2.1 MB"}],"format":"application/pdf","mimetype":"application/pdf","url":{"url":"https://fmu.repo.nii.ac.jp/record/2002088/files/FksmJMedSci_70_p11.pdf"},"version_id":"ce77c85f-428f-4553-a5c1-41f86790ad45"}]},"item_title":"Cellular carcinogenesis in preleukemic conditions: drivers and defenses","item_type_id":"40002","owner":"8","path":["1733193809282"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2024-02-01"},"publish_date":"2024-02-01","publish_status":"0","recid":"2002088","relation_version_is_last":true,"title":["Cellular carcinogenesis in preleukemic conditions: drivers and defenses"],"weko_creator_id":"8","weko_shared_id":-1},"updated":"2024-12-03T03:13:43.985198+00:00"}