{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T12:13:41Z","timestamp":1788351221932,"version":"build-2803163510"},"reference-count":159,"publisher":"Wiley","issue":"S4","license":[{"start":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T00:00:00Z","timestamp":1741651200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004948","name":"Astellas Pharma","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004948","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100019211","name":"AbbVie Canada","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100019211","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006436","name":"Celgene","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006436","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Alterations in the tumor suppressor gene\n                    <jats:italic>TP53<\/jats:italic>\n                    are common in human cancers and are associated with an aggressive nature. Approximately 8%\u201312% of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) harbor\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations (\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    ) and present immense challenges due to inherent chemoresistance and poor outcomes. As\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    are more common in older individuals and those with secondary\/therapy\u2010related myeloid neoplasms (MN), their incidence is expected to increase with an aging population and rising proportion of cancer survivors. Treatments used for other MN\u2014intensive chemotherapy, hypomethylating agents, and the BCL\u20102 inhibitor venetoclax\u2014do not improve the survival of\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    MN patients meaningfully. Additionally, further development of many promising agents has been discontinued, highlighting the challenges. Widespread acknowledgment of these problems led to the recognition of\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    MN as a distinct entity in the 5th edition of the World Health Organization and International Consensus Classifications. However, critical discrepancies between the two classifications may lead to under\u2010 or overestimation of the prognostic risk. Here, we review recent advances in the biology, diagnosis, and treatment of\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    MN. The development of\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    MN is positioned at the intersection of age, hereditary predisposition, and anti\u2010cancer therapies. Precursor\n                    <jats:italic>TP53<\/jats:italic>\n                    <jats:sup>mut<\/jats:sup>\n                    clones can be detected years prior to the eventual leukemic transformation\u2014raising the possibility of early intervention. We discuss the two classification systems and the bearing of the discrepancies between the two on timely and effective management. We provide novel evidence in the areas of discrepancies. Finally, we review the current therapeutic landscape and the obvious limitations of the currently used therapies.\n                  <\/jats:p>","DOI":"10.1002\/ajh.27655","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T08:38:47Z","timestamp":1741682327000},"page":"88-115","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["<scp>\n                      <i>TP53<\/i>\n                    <\/scp>\n                    \u2010Mutated Myeloid Neoplasms: 2024 Update on\u00a0Diagnosis, Risk\u2010Stratification, and Management"],"prefix":"10.1002","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5359-336X","authenticated-orcid":false,"given":"Mithun Vinod","family":"Shah","sequence":"first","affiliation":[{"name":"Division of Hematology Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2160-9689","authenticated-orcid":false,"given":"Daniel A.","family":"Arber","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Chicago  Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6666-3056","authenticated-orcid":false,"given":"Devendra K.","family":"Hiwase","sequence":"additional","affiliation":[{"name":"Department of Haematology, Royal Adelaide Hospital Central Adelaide Local Health Network  Adelaide South Australia Australia"},{"name":"Precision Medicine Theme South Australian Health and Medical Research Institute (SAHMRI)  Adelaide South Australia Australia"},{"name":"Adelaide Medical School University of Adelaide  Adelaide South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,3,11]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41568-020-0262-1"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1611604"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1013343"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature12634"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2024534"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1516192"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1200\/EDBK_432650"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.2021014472"},{"issue":"9","key":"e_1_2_12_10_1","first-page":"1087","article-title":"TP53 Mutation in Therapy\u2010Related Myeloid Neoplasm Defines a Distinct Molecular 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