{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:06:41Z","timestamp":1792033601020,"version":"4.4.0"},"reference-count":28,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T00:00:00Z","timestamp":1620259200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2021,7]]},"abstract":"Abstract<\/jats:title>\n \n Venetoclax (Ven) combined with a hypomethylating agent (HMA) has now emerged as an effective treatment regimen for acute myeloid leukemia, in both de novo and relapsed\/refractory setting. The current multicenter study retrospectively examined Ven\u2009+\u2009HMA treatment outcome among 32 patients (median age 69\u2009years; 59% males) with blast\u2010phase myeloproliferative neoplasm (MPN\u2010BP). Pre\u2010leukemic phenotype included essential thrombocythemia (ET)\/post\u2010ET myelofibrosis (34%), polycythemia vera (PV)\/post\u2010PV myelofibrosis (38%) and primary myelofibrosis (28%). Twenty\u2010nine study patients were fully annotated cytogenetically and molecularly (NGS): 69% harbored complex karyotype and\/or mutations, including\n TP53<\/jats:italic>\n (41%),\n IDH1\/2<\/jats:italic>\n (21%),\n ASXL1<\/jats:italic>\n (21%),\n N\/KRAS<\/jats:italic>\n (14%),\n SRSF2<\/jats:italic>\n (10%),\n EZH2<\/jats:italic>\n (10%) and\n U2AF1<\/jats:italic>\n (7%). All patients received Ven combined with either azacitidine (\n n<\/jats:italic>\n =\u200912) or decitabine (\n n<\/jats:italic>\n =\u200920); either up front (\n n<\/jats:italic>\n =\u200923) or after failing another induction therapy (\n n<\/jats:italic>\n =\u20099). Complete remission with (CR) or without (CRi) count recovery was achieved in 14 (44%) patients and was more likely to occur in the absence of pre\u2010leukemic PV\/post\u2010PV myelofibrosis phenotype (\n p<\/jats:italic>\n <\u2009.01), complex karyotype (\n p<\/jats:italic>\n <\u2009.01) or\n K\/NRAS<\/jats:italic>\n (\n p<\/jats:italic>\n =\u2009.03) mutations; seven of eight patients (88%) without vs four of 21 (19%) with complex karyotype or\n K\/NRAS<\/jats:italic>\n mutation achieved CR\/CRi (\n p<\/jats:italic>\n <\u2009.01); all 11 informative patients with pre\u2010leukemic PV\/post\u2010PV myelofibrosis phenotype displayed complex karyotype (\n p<\/jats:italic>\n <\u2009.01). In contrast, neither\n TP53<\/jats:italic>\n (\n p<\/jats:italic>\n =\u2009.45) nor\n IDH1\/2<\/jats:italic>\n (\n p<\/jats:italic>\n =\u2009.63) mutations affected response. Compared to historical controls treated with HMA alone (\n n<\/jats:italic>\n =\u200926), the CR\/CRi rate (44% vs 4%) and median survival (8 vs 5.5 months) were more favorable with Ven\u2009+\u2009HMA, but without significant difference in overall survival. Importantly, six patients with CR\/CRi subsequently received allogeneic hematopoietic stem cell transplant (AHSCT). Note, Ven\u2009+\u2009HMA produces robust CR\/CRi rates in MPN\u2010BP, especially in the absence of\n RAS<\/jats:italic>\n mutations and complex karyotype, thus enabling AHSCT, in some patients.\n <\/jats:p>","DOI":"10.1002\/ajh.26186","type":"journal-article","created":{"date-parts":[[2021,4,12]],"date-time":"2021-04-12T16:49:19Z","timestamp":1618246159000},"page":"781-789","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":69,"title":["Venetoclax with azacitidine or decitabine in blast\u2010phase myeloproliferative neoplasm: A multicenter series of 32 consecutive cases"],"prefix":"10.1002","volume":"96","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9104-6172","authenticated-orcid":false,"given":"Naseema","family":"Gangat","sequence":"first","affiliation":[{"name":"Division of Hematology Mayo Clinic Rochester Minnesota 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