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|Title:||C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia||Authors:||Alberich-Jordà, M.
|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. https://doi.org/10.1172/JCI65102||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||URI:||http://scholarbank.nus.edu.sg/handle/10635/125365||ISSN:||00219738||DOI:||10.1172/JCI65102|
|Appears in Collections:||Staff Publications|
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