{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T15:29:08Z","timestamp":1786980548134,"version":"build-2736575974"},"reference-count":72,"publisher":"Springer Science and Business Media LLC","issue":"7","license":[{"start":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T00:00:00Z","timestamp":1776384000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T00:00:00Z","timestamp":1776384000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/501100005611","name":"University of Fukui","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100005611","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Int J Clin Oncol"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Over the past decade, AML therapy has evolved from the uniform \u201c7\u2009+\u20093\u201d regimen toward a personalized approach. This transition integrates molecular genetic profiles with clinical fitness, driven by the genomic elucidation of AML and the development of selective targeted agents. Key advancements include the integration of FLT3 inhibitors into intensive chemotherapy and the emergence of venetoclax. When combined with hypomethylating agents, venetoclax has redefined the standard of care for older or unfit patients. Furthermore, IDH1\/2 inhibitors and menin inhibitors have provided potent options for molecular subsets defined by\n                    <jats:italic>IDH1\/2<\/jats:italic>\n                    mutations and\n                    <jats:italic>KMT2A<\/jats:italic>\n                    rearrangements or\n                    <jats:italic>NPM1<\/jats:italic>\n                    mutations, respectively. Innovations such as the liposomal formulation CPX-351 and oral formulations of CC-486 and oral decitabine\/cedazuridine have further optimized treatment delivery and improved patient quality of life. Despite these breakthroughs, intrinsic clonal heterogeneity and drug-resistant mutations, particularly\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation, remain significant challenges. Current research is actively exploring next-generation inhibitors, antibody\u2013drug conjugates, and cellular immunotherapies such as BiTEs and CAR-T cells. This review summarizes the recent pharmacological evolution in AML and discusses how these emerging therapies bring us closer to the ultimate goal of achieving a definitive cure.\n                  <\/jats:p>","DOI":"10.1007\/s10147-026-03038-7","type":"journal-article","created":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T13:24:37Z","timestamp":1776432277000},"page":"1151-1160","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The new era of AML therapy: current standards and emerging targets"],"prefix":"10.1007","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6336-3250","authenticated-orcid":false,"given":"Naoko","family":"Hosono","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,17]]},"reference":[{"key":"3038_CR1","doi-asserted-by":"publisher","first-page":"1136","DOI":"10.1056\/NEJMra1406184","volume":"373","author":"H D\u00f6hner","year":"2015","unstructured":"D\u00f6hner H, Weisdorf DJ, Bloomfield CD (2015) Acute myeloid leukemia. 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