Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia.
June TakedaKenichi YoshidaMasahiro Marshall NakagawaYasuhito NannyaAkinori YodaRyunosuke SaikiYotaro OchiLanying ZhaoRurika OkudaXingxing QiTakuto MoriAyana KonKenichi ChibaHiroko TanakaYuichi ShiraishiMing-Chung KuoCassandra M HirschYasunobu NagataDaisuke MorishitaNobuhiro HiramotoAkira HangaishiHideyuki NakazawaKen IshiyamaSatoru MiyanoShigeru ChibaYasushi MiyazakiToshiyuki KitanoKensuke UsukiNobuo SezakiHisashi TsurumiShuichi MiyawakiJaroslaw P MaciejewskiTakayuki IshikawaKazuma OhyashikiArnold GanserMichael HeuserFelicitas TholLee-Yung ShihAkifumi Takaori-KondoHideki MakishimaSeishi OgawaPublished in: Blood cancer discovery (2022)
This study reveals the major role of gains, amplifications, and mutations of EPOR and JAK2 in the pathogenesis of pure erythroleukemia. Their frequent response to ruxolitinib in patient-derived xenograft and cell culture models highlights a possible therapeutic role of JAK2 inhibition for erythroleukemia with EPOR/JAK2-involving lesions. This article is highlighted in the In This Issue feature, p. 369.