Truncating Erythropoietin Receptor Rearrangements in Acute Lymphoblastic Leukemia
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- 作者：Ilaria Iacobucci1 ; 19 ; Yongjin Li2 ; 19 ; Kathryn G. Roberts1 ; Stephanie M. Dobson3 ; Jaeseung C. Kim4 ; 5 ; Debbie Payne-Turner1 ; Richard C. Harvey6 ; Marcus Valentine7 ; Kelly McCastlain1 ; John Easton2 ; Donald Yergeau2 ; Laura J. Janke1 ; Ying Shao1 ; 2 ; I-Ming L. Chen6 ; Michael Rusch2 ; Sasan Zandi3 ; Steven M. Kornblau8 ; Marina Konopleva8 ; Elias Jabbour8 ; Elisabeth M. Paietta9 ; Jacob M. Rowe10 ; Ching-Hon Pui11 ; Julie Gastier-Foster12 ; Zhaohui Gu1 ; Shalini Reshmi12 ; Mignon L. Loh13 ; Janis Racevskis8 ; Martin S. Tallman14 ; Peter H. Wiernik15 ; Mark R. Litzow16 ; Cheryl L. Willman6 ; John D. McPherson17 ; James R. Downing1 ; Jinghui Zhang2 ; John E. Dick3 ; Stephen P. Hunger18 ; Charles G. Mullighan1 ; charles.mullighan@stjude.org" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cancer Cell
- 出版年：2016
- 出版时间：8 February 2016
- 年：2016
- 卷：29
- 期：2
- 页码：186-200
- 全文大小：5782 K
文摘
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Multiple EPOR rearrangements are recurrent in high-risk acute lymphoblastic leukemia
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EPOR rearrangements truncate the C terminus of EPOR and stabilize expression of the receptor
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Truncated EPOR is hypersensitive to EPO stimulation
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Truncated EPOR is leukemogenic and sensitive to JAK-STAT inhibition