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Title: Sox4 Is a Key Oncogenic Target in C/EBPα Mutant Acute Myeloid Leukemia
Authors: Zhang, H.
Alberich-Jorda, M.
Amabile, G.
Yang, H.
Staber, P.B.
DiRuscio, A.
Welner, R.S.
Ebralidze, A.
Zhang, J.
Levantini, E.
Lefebvre, V.
Valk, P.J.M.
Delwel, R.
Hoogenkamp, M.
Nerlov, C.
Cammenga, J.
Saez, B.
Scadden, D.T.
Bonifer, C.
Ye, M.
Tenen, D.G. 
Issue Date: 11-Nov-2013
Citation: Zhang, H., Alberich-Jorda, M., Amabile, G., Yang, H., Staber, P.B., DiRuscio, A., Welner, R.S., Ebralidze, A., Zhang, J., Levantini, E., Lefebvre, V., Valk, P.J.M., Delwel, R., Hoogenkamp, M., Nerlov, C., Cammenga, J., Saez, B., Scadden, D.T., Bonifer, C., Ye, M., Tenen, D.G. (2013-11-11). Sox4 Is a Key Oncogenic Target in C/EBPα Mutant Acute Myeloid Leukemia. Cancer Cell 24 (5) : 575-588. ScholarBank@NUS Repository.
Abstract: Mutation or epigenetic silencing of the transcription factor C/EBPα is observed in ~10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but downstream targets relevant for leukemogenesis are not known. Here, we identify Sox4 as a direct target of C/EBPα whereby its expression is inversely correlated with C/EBPα activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia-initiating cells (LICs) from both Sox4 overexpression and murine C/EBPα mutant AML models clustered together but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBPα inactivation contributes to the development of leukemia with a distinct LIC phenotype. © 2013 Elsevier Inc.
Source Title: Cancer Cell
ISSN: 15356108
DOI: 10.1016/j.ccr.2013.09.018
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