{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T19:53:52Z","timestamp":1774122832444,"version":"3.50.1"},"reference-count":167,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2025,2,27]],"date-time":"2025-02-27T00:00:00Z","timestamp":1740614400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institutes of Health","award":["R01 CA23741"],"award-info":[{"award-number":["R01 CA23741"]}]},{"name":"National Institutes of Health","award":["R01 HL 145780"],"award-info":[{"award-number":["R01 HL 145780"]}]},{"name":"National Institutes of Health","award":["R01 DK102943"],"award-info":[{"award-number":["R01 DK102943"]}]},{"name":"National Institutes of Health","award":["R01 HL143818"],"award-info":[{"award-number":["R01 HL143818"]}]},{"name":"MPN Research Fund","award":["R01 CA23741"],"award-info":[{"award-number":["R01 CA23741"]}]},{"name":"MPN Research Fund","award":["R01 HL 145780"],"award-info":[{"award-number":["R01 HL 145780"]}]},{"name":"MPN Research Fund","award":["R01 DK102943"],"award-info":[{"award-number":["R01 DK102943"]}]},{"name":"MPN Research Fund","award":["R01 HL143818"],"award-info":[{"award-number":["R01 HL143818"]}]},{"name":"Maryland Stem Cell Research Fund","award":["R01 CA23741"],"award-info":[{"award-number":["R01 CA23741"]}]},{"name":"Maryland Stem Cell Research Fund","award":["R01 HL 145780"],"award-info":[{"award-number":["R01 HL 145780"]}]},{"name":"Maryland Stem Cell Research Fund","award":["R01 DK102943"],"award-info":[{"award-number":["R01 DK102943"]}]},{"name":"Maryland Stem Cell Research Fund","award":["R01 HL143818"],"award-info":[{"award-number":["R01 HL143818"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Patients with chronic, indolent myeloproliferative neoplasms (MPNs) are at risk for transformation to highly lethal leukemia, although targetable mechanisms driving progression remain elusive. We discovered that the High Mobility Group A1 (HMGA1) gene is up-regulated with MPN progression in patients and required for evolution into myelofibrosis (MF) or acute myeloid leukemia (AML) in preclinical models. HMGA1 encodes the HMGA1 epigenetic regulators that modulate the chromatin state during embryogenesis and tissue regeneration. While HMGA1 is silenced in most differentiated cells, it becomes aberrantly re-expressed in JAK2 mutant (JAK2-V617F) MPN, with the highest levels after transformation to secondary MF or AML. Here, we review recent work highlighting HMGA1 function in MPN progression. Though underlying mechanisms continue to emerge, increasing evidence suggests that HMGA1 functions as a \u201cchromatin key\u201d required to \u201cunlock\u201d regions of the genome involved in clonal expansion and progression in MPN. Together, these findings illuminate HMGA1 as a driver of MPN progression and a promising therapeutic target.<\/jats:p>","DOI":"10.3390\/ijms26052125","type":"journal-article","created":{"date-parts":[[2025,2,28]],"date-time":"2025-02-28T02:48:37Z","timestamp":1740710917000},"page":"2125","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["High Mobility Group A1 Chromatin Keys: Unlocking the Genome During MPN Progression"],"prefix":"10.3390","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4004-7060","authenticated-orcid":false,"given":"Linda M. S.","family":"Resar","sequence":"first","affiliation":[{"name":"Departments of Medicine (Hematology), Oncology, Pathology and Institute for Cellular Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8680-4119","authenticated-orcid":false,"given":"Li Z.","family":"Luo","sequence":"additional","affiliation":[{"name":"Departments of Medicine (Hematology), Oncology, Pathology and Institute for Cellular Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,2,27]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"31","DOI":"10.1158\/2159-8290.CD-21-1059","article-title":"Hallmarks of Cancer: New Dimensions","volume":"12","author":"Hanahan","year":"2022","journal-title":"Cancer Discov."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"387","DOI":"10.1038\/s41586-022-05365-x","article-title":"Subtype-Specific 3D Genome Alteration in Acute Myeloid Leukaemia","volume":"611","author":"Xu","year":"2022","journal-title":"Nature"},{"key":"ref_3","doi-asserted-by":"crossref","unstructured":"Sobo, J.M., Alagna, N.S., Sun, S.X., Wilson, K.L., and Reddy, K.L. 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