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Blood, 15 August 2004, Vol. 104, No. 4, pp. 1204-1209. Prepublished online as a Blood First Edition Paper on April 27, 2004; DOI 10.1182/blood-2004-03-1094. This Article Full Text (PDF) All Versions of this Article: 2004-03-1094v1 104/4/1204    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 Clapp, D W Search for Related Content PubMed PubMed Citation Articles by Li, X. Articles by Clapp, D W Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 23, 2004 Accepted March 25, 2004 Continuous in vivo infusion of Interferon-gamma (IFN-) preferentially reduces myeloid progenitor numbers and enhances engraftment of syngeneic wildtype cells in Fancc-/- mice Xiaxin Li, Yanzhu Yang, Jin Yuan, Ping Hong, Brian Freie, Attilio Orazi, Laura S Haneline, and D W Clapp* Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Microbiology/Immunology, Indiana University School of Medicine, Indianapolis, IN, USA * Corresponding author; email: dclapp{at}iupui.edu. Fanconi anemia (FA) is characterized by bone marrow (BM) failure and cancer susceptibility. Identification of the cDNAs of many FA complementation types allows the potential of using gene transfer technology to introduce functional cDNAs as transgenes into autologous stem cells and provide a cure for the BM failure in FA patients. Previous studies in FA murine models and in a phase I clinical trial suggest that myelopreparation is required for significant engraftment of exogenous, genetically-corrected, stem cells. Since myeloid progenitors from Fancc -/- mice and human FANCC patients have increased apoptosis in response to IFN- in vitro, we hypothesized that IFN- may be useful as a non-genotoxic, myelopreparative, conditioning agent. To test this hypothesis, IFN- was administered as a continuous infusion to Fancc -/- and wildtype (WT) mice for 1 week. Primitive and mature myeloid lineages were preferentially reduced in IFN- treated Fancc -/- mice. Further, IFN- conditioning of Fancc -/- recipients was sufficient as a myelopreparative regimen to allow consistent engraftment of isogenic WT repopulating stem cells. Collectively, these data demonstrate that Fancc -/- hematopoietic cell populations have increased hypersensitivity to IFN- in vivo and that IFN- conditioning may be useful as a non-genotoxic strategy for myelopreparation in this disorder. 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] P. Rio, N. W. Meza, A. Gonzalez-Murillo, S. Navarro, L. Alvarez, J. Surralles, M. Castella, G. Guenechea, J. C. Segovia, H. Hanenberg, et al. In vivo proliferation advantage of genetically corrected hematopoietic stem cells in a mouse model of Fanconi anemia FA-D1 Blood, December 15, 2008; 112(13): 4853 - 4861. [Abstract] [Full Text] [PDF] X. Zhang, X. Shang, F. Guo, K. Murphy, M. Kirby, P. Kelly, L. Reeves, F. O. Smith, D. A. Williams, Y. Zheng, et al. Defective homing is associated with altered Cdc42 activity in cells from patients with Fanconi anemia group A Blood, September 1, 2008; 112(5): 1683 - 1686. [Abstract] [Full Text] [PDF] X. Zhang, D. P. Sejas, Y. Qiu, D. A. Williams, and Q. Pang Inflammatory ROS promote and cooperate with the Fanconi anemia mutation for hematopoietic senescence J. Cell Sci., May 1, 2007; 120(9): 1572 - 1583. [Abstract] [Full Text] [PDF] D. P. Sejas, R. Rani, Y. Qiu, X. Zhang, S. R. Fagerlie, H. Nakano, D. A. Williams, and Q. Pang Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient Mice J. Immunol., April 15, 2007; 178(8): 5277 - 5287. [Abstract] [Full Text] [PDF] Y. Si, S. Ciccone, F.-C. Yang, J. Yuan, D. Zeng, S. Chen, H. J. van de Vrugt, J. Critser, F. Arwert, L. S. Haneline, et al. Continuous in vivo infusion of interferon-gamma (IFN-{gamma}) enhances engraftment of syngeneic wild-type cells in Fanca-/- and Fancg-/- mice Blood, December 15, 2006; 108(13): 4283 - 4287. [Abstract] [Full Text] [PDF] K. Bijangi-Vishehsaraei, M. R. Saadatzadeh, A. Werne, K. A. W. McKenzie, R. Kapur, H. Ichijo, and L. S. Haneline Enhanced TNF-{alpha}-induced apoptosis in Fanconi anemia type C-deficient cells is dependent on apoptosis signal-regulating kinase 1 Blood, December 15, 2005; 106(13): 4124 - 4130. [Abstract] [Full Text] [PDF] S. Schubbert, K. Lieuw, S. L. Rowe, C. M. Lee, X. Li, M. L. Loh, D. W. Clapp, and K. M. Shannon Functional analysis of leukemia-associated PTPN11 mutations in primary hematopoietic cells Blood, July 1, 2005; 106(1): 311 - 317. [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]

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