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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2631-2640. Prepublished online as a Blood First Edition Paper on June 22, 2007; DOI 10.1182/blood-2006-10-053850. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-10-053850v1 110/7/2631    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Cui, J.-W. Articles by Ben-David, Y. Search for Related Content PubMed PubMed Citation Articles by Cui, J.-W. Articles by Ben-David, Y. Related Collections Oncogenes and Tumor Suppressors Signal Transduction Gene Expression Hematopoiesis and Stem Cells Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Retroviral insertional activation of the Fli-3 locus in erythroleukemias encoding a cluster of microRNAs that convert Epo-induced differentiation to proliferation Jiu-Wei Cui1,2, You-Jun Li1,3, Aloke Sarkar1,3, Jeremy Brown1, Ye-Hui Tan2, Marina Premyslova1, Crystal Michaud1, Norman Iscove3, Guan-Jun Wang2, and Yaacov Ben-David1,3 1 Department of Molecular and Cellular Biology, Sunnybrook Health Sciences Center, Toronto, ON; 2 Department of Hematology, the First Hospital of Jilin University, Changchun, China; 3 Department of Medical Biophysics, University of Toronto, ON MicroRNAs (miRNAs) are a newly discovered class of posttranscriptional regulatory noncoding small RNAs. Recent evidence has shown that miRNA misexpression correlates with progression of various human cancers. Friend erythroleukemia has been used as an excellent system for the identification and characterization of oncogenes and tumor suppressor genes involved in neoplastic transformation. Using this model, we have isolated a novel integration site designated Fli-3, from a Friend murine leukemia virus (F-MuLV)–induced erythroleukemia. The Fli-3 transcription unit is a murine homologue of the human gene C13orf25 that includes a region encoding the mir-17–92 miRNA cluster. C13orf25 is the target gene of 13q31 chromosomal amplification in human B-cell lymphomas and other malignancies. The erythroleukemias that have acquired either insertional activation or amplification of Fli-3 express higher levels of the primary or mature miRNAs derived from mir-17–92. The ectopic expression of Fli-3 in an erythroblastic cell line switches erythropoietin (Epo)–induced differentiation to Epo-induced proliferation through activation of the Ras and PI3K pathways. Such a response is associated with alteration in the expression of several regulatory factors, such as Spi-1 and p27 (Kip1). These findings highlight the potential of the Fli-3 encoding mir-17–92 in the development of erythroleukemia and its important role in hematopoiesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Scherr, L. Venturini, K. Battmer, M. Schaller-Schoenitz, D. Schaefer, I. Dallmann, A. Ganser, and M. Eder Lentivirus-mediated antagomir expression for specific inhibition of miRNA function Nucleic Acids Res., December 3, 2007; 35(22): e149 - e149. [Abstract] [Full Text] [PDF]

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