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This Article Full Text Full Text (PDF) 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 Tschan, C. A. Articles by Germeshausen, M. Search for Related Content PubMed PubMed Citation Articles by Tschan, C. A. Articles by Germeshausen, M. Related Collections Hematopoiesis and Stem Cells Neoplasia Phagocytes Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 March 2001, Vol. 97, No. 6, pp. 1882-1884 BRIEF REPORT Time course of increasing numbers of mutations in the granulocyte colony-stimulating factor receptor gene in a patient with congenital neutropenia who developed leukemia Christoph A. Tschan, Christina Pilz, Cornelia Zeidler, Karl Welte, and Manuela Germeshausen From the Department of Paediatric Haematology and Oncology, Hannover Medical School Hannover, Germany. Point mutations in the granulocyte colony-stimulating factor receptor (G-CSFR) gene have been linked to the development of secondary leukemia in patients with congenital neutropenia (CN). This report presents data on a now 18-year-old patient with CN who has received G-CSF treatment since 1989 and who developed acute myeloid leukemia (AML) in 1998. To evaluate whether there is an association between the occurrence of point mutations of the G-CSFR gene and development of secondary AML, DNA/messenger RNA of neutrophils and mononuclear cells from this patient were analyzed at different time points by polymerase chain reaction and subsequent cloning by DNA sequencing of representative numbers of individual clones. Findings suggest an increasing instability of the G-CSFR gene in time as judged by increasing numbers of mutations proposed to be one important step in the development of AML in this patient. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Germeshausen, M. Ballmaier, and K. Welte Incidence of CSF3R mutations in severe congenital neutropenia and relevance for leukemogenesis: results of a long-term survey Blood, January 1, 2007; 109(1): 93 - 99. [Abstract] [Full Text] [PDF] P. S. Rosenberg, B. P. Alter, A. A. Bolyard, M. A. Bonilla, L. A. Boxer, B. Cham, C. Fier, M. Freedman, G. Kannourakis, S. Kinsey, et al. The incidence of leukemia and mortality from sepsis in patients with severe congenital neutropenia receiving long-term G-CSF therapy Blood, June 15, 2006; 107(12): 4628 - 4635. [Abstract] [Full Text] [PDF] T. Mitsui, S. Watanabe, Y. Taniguchi, S. Hanada, Y. Ebihara, T. Sato, T. Heike, M. Mitsuyama, T. Nakahata, and K. Tsuji Impaired neutrophil maturation in truncated murine G-CSF receptor-transgenic mice Blood, April 15, 2003; 101(8): 2990 - 2995. [Abstract] [Full Text] [PDF]

	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020