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Title: C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia
Authors: Alberich-Jordà, M.
Wouters, B.
Balastik, M.
Shapiro-Koss, C.
Zhang, H.
DiRuscio, A.
Radomska, H.S.
Ebralidze, A.K.
Amabile, G.
Ye, M.
Zhang, J.
Lowers, I.
Avellino, R.
Melnick, A.
Figueroa, M.E.
Valk, P.J.M.
Delwel, R.
Tenen, D.G. 
Issue Date: 3-Dec-2012
Citation: Alberich-Jordà, M., Wouters, B., Balastik, M., Shapiro-Koss, C., Zhang, H., DiRuscio, A., Radomska, H.S., Ebralidze, A.K., Amabile, G., Ye, M., Zhang, J., Lowers, I., Avellino, R., Melnick, A., Figueroa, M.E., Valk, P.J.M., Delwel, R., Tenen, D.G. (2012-12-03). C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia. Journal of Clinical Investigation 122 (12) : 4490-4504. ScholarBank@NUS Repository.
Abstract: C/EBPs are a family of transcription factors that regulate growth control and differentiation of various tissues. We found that C/EBPγ is highly upregulated in a subset of acute myeloid leukemia (AML) samples characterized by C/EBPα hypermethylation/silencing. Similarly, C/EBPγ was upregulated in murine hematopoietic stem/progenitor cells lacking C/EBPα, as C/EBPα mediates C/EBPγ suppression. Studies in myeloid cells demonstrated that CEBPG overexpression blocked neutrophilic differentiation. Further, downregulation of Cebpg in murine Cebpa-deficient stem/progenitor cells or in human CEBPA-silenced AML samples restored granulocytic differentiation. In addition, treatment of these leukemias with demethylating agents restored the C/EBPα-C/EBPγ balance and upregulated the expression of myeloid differentiation markers. Our results indicate that C/EBPγ mediates the myeloid differentiation arrest induced by C/EBPα deficiency and that targeting the C/EBPα-C/EBPγ axis rescues neutrophilic differentiation in this unique subset of AMLs.
Source Title: Journal of Clinical Investigation
ISSN: 00219738
DOI: 10.1172/JCI65102
Appears in Collections:Staff Publications

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