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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2827-2836. Prepublished online as a Blood First Edition Paper on June 28, 2005; DOI 10.1182/blood-2005-01-0358. This Article Full Text (PDF) Supplemental Table All Versions of this Article: 2005-01-0358v1 106/8/2827    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gery, S. Articles by Koeffler, H P Search for Related Content PubMed PubMed Citation Articles by Gery, S. Articles by Koeffler, H P Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 27, 2005 Accepted June 6, 2005 Transcription profiling of C/EBP targets identifies Per2 as a gene implicated in myeloid leukemia Sigal Gery*, Adrian F Gombart, William S Yi, Chloe Koeffler, Wolf K Hofmann, and H P Koeffler Cedars-Sinai Medical Center, Division of Hematology/Oncology, UCLA School of Medicine, Los Angeles, CA, USA Department of Hematology and Oncology and Transfusion Medicine, University Hospital "Benjamin Franklin", Berlin, Germany * Corresponding author; email: gerys{at}cshs.org. CCAAT/enhancer-binding proteins (C/EBPs) are a family of transcription factors that regulate cell growth and differentiation in numerous cell types. To identify novel C/EBP-target genes, we performed transcriptional profiling using inducible NIH 3T3 cell lines expressing one of four members of the C/EBP family. Functional analysis revealed a previously unknown link between C/EBP proteins and circadian clock genes. Our microarray data showed that the expression levels of two core components of the circadian network, Per2 and Rev-Erb, were significantly altered by C/EBPs. Recent studies suggested that Per2 behaves as a tumor suppressor gene in mice. Therefore, we focused our additional studies on Per2. We showed that Per2 expression is upregulated by C/EBP and C/EBP. Per2 levels were reduced in lymphoma cell lines and in acute myeloid leukemia (AML) patient samples. In addition, we generated stable K562 cells that expressed an inducible Per2 gene. Induction of Per2 expression resulted in growth inhibition, cell cycle arrest, apoptosis and loss of clonogenic ability. These results suggest that Per2 is a downstream C/EBP-target gene involved in AML, and its disruption might be involved in initiation and/or progression of AML. 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