{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T11:07:44Z","timestamp":1780484864232,"version":"3.54.1"},"reference-count":26,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2020,12,21]],"date-time":"2020-12-21T00:00:00Z","timestamp":1608508800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP16K19203"],"award-info":[{"award-number":["JP16K19203"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP15K15368"],"award-info":[{"award-number":["JP15K15368"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Discrimination of Philadelphia\u2010negative myeloproliferative neoplasms (Ph\u2010MPNs) from reactive hypercytosis and myelofibrosis requires a constellation of testing including driver mutation analysis and bone marrow biopsies. We searched for a biomarker that can more easily distinguish Ph\u2010MPNs from reactive hypercytosis and myelofibrosis by using RNA\u2010seq analysis utilizing platelet\u2010rich plasma (PRP)\u2010derived RNAs from patients with essential thrombocythemia (ET) and reactive thrombocytosis, and <jats:italic>CREB3L1<\/jats:italic> was found to have an extremely high impact in discriminating the two disorders. To validate and further explore the result, expression levels of <jats:italic>CREB3L1<\/jats:italic> in PRP were quantified by reverse\u2010transcription quantitative PCR and compared among patients with ET, other Ph\u2010MPNs, chronic myeloid leukemia (CML), and reactive hypercytosis and myelofibrosis. A <jats:italic>CREB3L1<\/jats:italic> expression cutoff value determined based on PRP of 18 healthy volunteers accurately discriminated 150 driver mutation\u2013positive Ph\u2010MPNs from other entities (71 reactive hypercytosis and myelofibrosis, 6 CML, and 18 healthy volunteers) and showed both sensitivity and specificity of 1.0000. Importantly, <jats:italic>CREB3L1<\/jats:italic> expression levels were significantly higher in ET compared with reactive thrombocytosis (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.0001), and polycythemia vera compared with reactive erythrocytosis (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.0001). Pathology\u2010affirmed triple\u2010negative ET (TN\u2010ET) patients were divided into a high\u2013 and low\u2013<jats:italic>CREB3L1\u2010<\/jats:italic>expression group, and some patients in the low\u2010expression group achieved a spontaneous remission during the clinical course. In conclusion, <jats:italic>CREB3L1<\/jats:italic> analysis has the potential to single\u2010handedly discriminate driver mutation\u2013positive Ph\u2010MPNs from reactive hypercytosis and myelofibrosis, and also may identify a subgroup within TN\u2010ET showing distinct clinical features including spontaneous remission.<\/jats:p>","DOI":"10.1111\/cas.14763","type":"journal-article","created":{"date-parts":[[2020,12,6]],"date-time":"2020-12-06T10:22:03Z","timestamp":1607250123000},"page":"884-892","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["<i>CREB3L1<\/i> overexpression as a potential diagnostic marker of Philadelphia chromosome\u2013negative myeloproliferative neoplasms"],"prefix":"10.1111","volume":"112","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1081-0130","authenticated-orcid":false,"given":"Soji","family":"Morishita","sequence":"first","affiliation":[{"name":"Department of Transfusion Medicine 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