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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2003-02-0536. This Article Full Text (PDF) All Versions of this Article: 2003-02-0536v1 102/6/2081    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 Li, X. Articles by Haneline, L. S Search for Related Content PubMed PubMed Citation Articles by Li, X. Articles by Haneline, L. S Social Bookmarking                   What's this? Submitted February 19, 2003 Accepted May 10, 2003 Fanconi anemia type C deficient hematopoietic stem/progenitor cells exhibit aberrant cell cycle control Xiaxin Li, P Artur Plett, Yanzhu Yang, Ping Hong, Brian Freie, Edward F Srour, Christie M Orschell, D Wade Clapp, and Laura S Haneline* Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA Department of Microbiology/Immunology, Indiana University School of Medicine, Indianapolis, IN, USA * Corresponding author; email: lhanelin{at}iupui.edu. The pathogenesis of bone marrow failure in Fanconi anemia is poorly understood. Suggested mechanisms include enhanced apoptosis secondary to DNA damage and altered inhibitory cytokine signaling. Recent data determined that disrupted cell cycle control of hematopoietic stem and /or progenitor cells disrupts normal hematopoiesis with increased hematopoietic stem cell cycling resulting in diminished function and increased sensitivity to cell cycle specific, apoptotic stimuli. Here, we utilized Fanconi anemia complementation type C deficient (Fancc -/-) mice to demonstrate that Fancc -/- phenotypically-defined cell populations enriched for hematopoietic stem and progenitor cells exhibit increased cycling. In addition, we established that the defect in cell cycle regulation is not a compensatory mechanism from enhanced apoptosis occurring in vivo. Collectively, these data provide a previously unrecognized phenotype in Fancc -/- hematopoietic stem/progenitor cells, which may contribute to the progressive bone marrow failure in Fanconi anemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Li, S. Chen, J. Yuan, Y. Yang, J. Li, J. Ma, X. Wu, M. Freund, K. Pollok, H. Hanenberg, et al. Mesenchymal stem/progenitor cells promote the reconstitution of exogenous hematopoietic stem cells in Fancg-/- mice in vivo Blood, March 5, 2009; 113(10): 2342 - 2351. [Abstract] [Full Text] [PDF] C. S. Tremblay, F. F. Huang, O. Habi, C. C. Huard, C. Godin, G. Levesque, and M. Carreau HES1 is a novel interactor of the Fanconi anemia core complex Blood, September 1, 2008; 112(5): 2062 - 2070. [Abstract] [Full Text] [PDF] X. Li, M. M. Le Beau, S. Ciccone, F.-C. Yang, B. Freie, S. Chen, J. Yuan, P. Hong, A. Orazi, L. S. Haneline, et al. Ex vivo culture of Fancc-/- stem/progenitor cells predisposes cells to undergo apoptosis, and surviving stem/progenitor cells display cytogenetic abnormalities and an increased risk of malignancy Blood, May 1, 2005; 105(9): 3465 - 3471. [Abstract] [Full Text] [PDF] S. Franco, H. J. van de Vrugt, P. Fernandez, M. Aracil, F. Arwert, and M. A. Blasco Telomere dynamics in Fancg-deficient mouse and human cells Blood, December 15, 2004; 104(13): 3927 - 3935. [Abstract] [Full Text] [PDF]

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