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Vol.70 (2024) >

Please use this identifier to cite or link to this item: http://ir.fmu.ac.jp/dspace/handle/123456789/2209

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Title: Cellular carcinogenesis in preleukemic conditions: drivers and defenses
Authors: Ueda, Koki
Ikeda, Kazuhiko
Affiliation: 輸血・移植免疫学講座
Source title: Fukushima Journal of Medical Science
Volume: 70
Issue: 1
Start page: 11
End page: 24
Issue Date: 2024
Abstract: 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.
Publisher: The Fukushima Society of Medical Science
Publisher (Alternative foam): 福島医学会
language: eng
URI: http://ir.fmu.ac.jp/dspace/handle/123456789/2209
Full text URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/2209/1/FksmJMedSci_70_p11.pdf
ISSN: 0016-2590
2185-4610
DOI: 10.5387/fms.2023-17
PubMed ID: 37952978
Related Page: https://doi.org/10.5387/fms.2023-17
Rights: © 2024 The Fukushima Society of Medical Science. This article is licensed under a Creative Commons [Attribution-NonCommercial-ShareAlike 4.0 International] license.
Rights: https://creativecommons.org/licenses/by-nc-sa/4.0/
Appears in Collections:Vol.70 (2024)

Files in This Item:

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FksmJMedSci_70_p11.pdf2.14 MBAdobe PDFDownload

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