{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T16:35:30Z","timestamp":1783528530257,"version":"3.55.0"},"reference-count":25,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2020,10,22]],"date-time":"2020-10-22T00:00:00Z","timestamp":1603324800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,2,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Objectives<\/jats:title>\n                  <jats:p>Hypocellular acute myeloid leukemia (AML) is uncommon. Despite the prognostic and therapeutic importance of mutational analysis, the mutational landscape of hypocellular AML is not well understood.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>We identified 25 patients with hypocellular AML, and 141 patients with nonhypocellular AML were identified as a control group. We applied next-generation sequencing for the first time to profile this entity.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The hypocellular AML patients were older than those with nonhypocellular AML (P = .037). At diagnosis, hypocellular AML had lower leukocyte counts (P = .012), higher hemoglobin (P = .003), and lower blast counts in the peripheral blood (P &amp;lt; .001) and bone marrow (P = .003). Hypocellular AML was less likely to have mutations involving cell proliferation (P = .027) and NPM1 (P = .022) compared with nonhypocellular AML. Hypocellular AML showed a high incidence of spliceosomal mutations and myelodysplastic syndrome-defining chromosome abnormalities (65%), but the incidence was not significantly different from that in nonhypocellular AML. There was no significant survival difference between hypocellular and nonhypocellular AML.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>To our knowledge, this study is the first to demonstrate hypocellular AML showed fewer genetic alterations involving cell proliferation and NPM1 when compared directly with nonhypocellular AML; this finding likely contributes to the low marrow cellularity in at least a portion of the patients with hypocellular AML.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ajcp\/aqaa150","type":"journal-article","created":{"date-parts":[[2020,7,31]],"date-time":"2020-07-31T19:11:51Z","timestamp":1596222711000},"page":"446-454","source":"Crossref","is-referenced-by-count":3,"title":["Clinicopathologic Characterization of Hypocellular Acute Myeloid Leukemia (AML) Showed Fewer Genetic Abnormalities Involving Cell Proliferation and <i>NPM1<\/i> When Compared With Nonhypocellular AML"],"prefix":"10.1093","volume":"155","author":[{"given":"Eric","family":"Carlsen","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathanael G","family":"Bailey","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nidhi","family":"Aggarwal","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gwendolyn 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