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Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2003-02-0490. This Article Full Text (PDF) All Versions of this Article: 2003-02-0490v1 103/1/325    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 Zeng, W. Articles by Young, N. S Search for Related Content PubMed PubMed Citation Articles by Zeng, W. Articles by Young, N. S Social Bookmarking                   What's this? Submitted February 13, 2003 Accepted September 6, 2003 Gene expression profiling in CD34 cells identifies significant differences between aplastic anemia patients and health volunteers Weihua Zeng*, Guibin Chen, Sachiko Kajigaya, Olga Nunez, Alexandra Charrow, Eric M Billings, and Neal S Young Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA * Corresponding author; email: zengw{at}nhlbi.nih.gov. An immune pathophysiology for acquired aplastic anemia (AA) has been inferred from the responsiveness of the patients to immunosuppressive therapies and experimental laboratory data. To address the transcriptome of hematopoietic cells in AA, we undertook GeneChip analysis of the extremely limited numbers of progenitor and stem cells in the marrow of patients with this disease. We pooled total RNA from highly enriched bone marrow CD34 cells of 36 newly diagnosed AA patients and 12 normal volunteers for analysis on Affymetrix oligonucleotide chips (Human Genome U95A version 2 Array). A large number of genes implicated in apoptosis and cell death showed markedly increased expression in AA CD34 cells, and negative proliferation control genes also had increased activity. Conversely, cell cycle progress-enhancing genes showed low expression in AA. Cytokine/chemokine signal transducer genes, stress response genes, and defense/immune response genes were up-regulated, as anticipated from other evidence of the heightened immune activity in AA patients' marrow. In summary, detailed genetic analysis of small numbers of hematopoietic progenitor cells is feasible even in marrow failure states where such cells are present in very small numbers. The gene expression profile of primary human CD34 hematopoietic stem cells from AA was consistent with a stressed, dying, and immunologically activated target cell population. Many of the genes showing differential expression in AA deserve further detailed analysis, including comparison with other marrow failure states and autoimmune disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. K. Ahn, H.-S. Cha, E.-M. Koh, S.-H. Kim, Y. G. Kim, C.-K. Lee, and B. Yoo Behcet's disease associated with bone marrow failure in Korean patients: clinical characteristics and the association of intestinal ulceration and trisomy 8 Rheumatology, August 1, 2008; 47(8): 1228 - 1230. [Abstract] [Full Text] [PDF] N. S. Young, R. T. Calado, and P. Scheinberg Current concepts in the pathophysiology and treatment of aplastic anemia Blood, October 15, 2006; 108(8): 2509 - 2519. [Abstract] [Full Text] [PDF] A. 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