Instructive Role of MLL-Fusion Proteins Revealed by a Model of t(4;11) Pro-B Acute Lymphoblastic Leukemia
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- 作者：Shan Lin1 ; 6 ; Roger T. Luo2 ; 6 ; Anetta Ptasinska3 ; Jon Kerry4 ; Salam A. Assi3 ; Mark Wunderlich1 ; Toshihiko Imamura2 ; Joseph J. Kaberlein2 ; Ahmad Rayes1 ; Mark J. Althoff1 ; John Anastasi5 ; Maureen M. O&rsquo ; Brien1 ; Amom Ruhikanta Meetei1 ; Thomas A. Milne4 ; Constanze Bonifer3 ; James C. Mulloy1 ; james.mulloy@cchmc.org" class="auth_mail" title="E-mail the corresponding author ; Michael J. Thirman2 ; 7 ; mthirman@medicine.bsd.uchicago.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：MLL-AF4 ; acute lymphoblastic leukemia ; chimeric fusion proteins ; mouse models of cancer ; acquired resistance to targeted therapy ; species specificity of oncogenes
- 刊名：Cancer Cell
- 出版年：2016
- 出版时间：14 November 2016
- 年：2016
- 卷：30
- 期：5
- 页码：737-749
- 全文大小：5759 K
文摘
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Fusion of MLL to murine Af4 permits faithful modeling of human t(4;11) pro-B ALL
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The species of the cell-of-origin determines the lineage of MLL-Af4 leukemia
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MLL-fusion proteins drive differential gene expression via specific DNA binding
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MLL-fusion leukemia circumvents CD19-directed therapies through lineage plasticity