Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ccr.2013.09.018
DC FieldValue
dc.titleSox4 Is a Key Oncogenic Target in C/EBPα Mutant Acute Myeloid Leukemia
dc.contributor.authorZhang, H.
dc.contributor.authorAlberich-Jorda, M.
dc.contributor.authorAmabile, G.
dc.contributor.authorYang, H.
dc.contributor.authorStaber, P.B.
dc.contributor.authorDiRuscio, A.
dc.contributor.authorWelner, R.S.
dc.contributor.authorEbralidze, A.
dc.contributor.authorZhang, J.
dc.contributor.authorLevantini, E.
dc.contributor.authorLefebvre, V.
dc.contributor.authorValk, P.J.M.
dc.contributor.authorDelwel, R.
dc.contributor.authorHoogenkamp, M.
dc.contributor.authorNerlov, C.
dc.contributor.authorCammenga, J.
dc.contributor.authorSaez, B.
dc.contributor.authorScadden, D.T.
dc.contributor.authorBonifer, C.
dc.contributor.authorYe, M.
dc.contributor.authorTenen, D.G.
dc.date.accessioned2016-07-08T09:27:16Z
dc.date.available2016-07-08T09:27:16Z
dc.date.issued2013-11-11
dc.identifier.citationZhang, 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. https://doi.org/10.1016/j.ccr.2013.09.018
dc.identifier.issn15356108
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/125455
dc.description.abstractMutation 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.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.ccr.2013.09.018
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMEDICINE
dc.description.doi10.1016/j.ccr.2013.09.018
dc.description.sourcetitleCancer Cell
dc.description.volume24
dc.description.issue5
dc.description.page575-588
dc.description.codenCCAEC
dc.identifier.isiut000327005100006
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.