{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T12:39:06Z","timestamp":1792931946809,"version":"4.5.0"},"reference-count":51,"publisher":"Springer Science and Business Media LLC","issue":"9","license":[{"start":{"date-parts":[[2024,7,20]],"date-time":"2024-07-20T00:00:00Z","timestamp":1721433600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2024,7,20]],"date-time":"2024-07-20T00:00:00Z","timestamp":1721433600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Ann Hematol"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Therapy-related myeloid neoplasms (t-MN) are characterized by aggressive features and a dismal prognosis. Recent evidence suggests a higher incidence of t-MN in individuals harboring clonal hematopoiesis of indeterminate potential (CHIP). In order to gain insight into CHIP-driven malignant progression, we gathered data from ten published reports with available detailed patient characteristics at the time of primary malignancy and t-MN development. Detailed clinical and molecular information on primary malignancy and t-MN were available for 109 patients: 43% harbored at least one somatic mutation at the time of the primary malignancy.\n                    <jats:italic>TET2<\/jats:italic>\n                    and\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations showed an increasing variant allele frequency from CHIP to t-MN.\n                    <jats:italic>ASXL1<\/jats:italic>\n                    -associated CHIP significantly correlated with the emergence of\n                    <jats:italic>TET2<\/jats:italic>\n                    and\n                    <jats:italic>CEBPA<\/jats:italic>\n                    mutations at t-MN, as well as\n                    <jats:italic>U2AF1<\/jats:italic>\n                    -driven\n                    <jats:italic>CHIP<\/jats:italic>\n                    with\n                    <jats:italic>EZH2<\/jats:italic>\n                    mutation and both\n                    <jats:italic>IDH2<\/jats:italic>\n                    and\n                    <jats:italic>SRSF2<\/jats:italic>\n                    -driven CHIP with\n                    <jats:italic>FLT3<\/jats:italic>\n                    mutation.\n                    <jats:italic>DNMT3A<\/jats:italic>\n                    -driven CHIP correlated with a lower incidence of\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation at t-MN. In contrast,\n                    <jats:italic>TP53<\/jats:italic>\n                    -driven CHIP correlated with a complex karyotype and a lower tendency to acquire new mutations at t-MN. Patients with multiple myeloma as their first malignancy presented a significantly higher rate of\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations at t-MN. The progression from CHIP to t-MN shows different scenarios depending on the genes involved. A deeper knowledge of CHIP progression mechanisms will allow a more reliable definition of t-MN risk.\n                  <\/jats:p>","DOI":"10.1007\/s00277-024-05803-y","type":"journal-article","created":{"date-parts":[[2024,7,20]],"date-time":"2024-07-20T02:01:50Z","timestamp":1721440910000},"page":"3507-3517","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["The role of clonal progression leading to the development of therapy-related myeloid neoplasms"],"prefix":"10.1007","volume":"103","author":[{"given":"Luca","family":"Guarnera","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Rosaria","family":"Pascale","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajro","family":"Hajrullaj","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio","family":"Cristiano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flavia","family":"Mallegni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelo","family":"Onorato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Teresa","family":"Voso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emiliano","family":"Fabiani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,7,20]]},"reference":[{"key":"5803_CR1","doi-asserted-by":"crossref","unstructured":"Khoury JD et al (2022) The 5th edition of the World Health Organization classification of haematolymphoid tumours: myeloid and histiocytic\/dendritic neoplasms. 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