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This Article Order Full text via Infotrieve 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 Cooper, B. Articles by Breg, W. R. Search for Related Content PubMed PubMed Citation Articles by Cooper, B. Articles by Breg, W. R. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Loss of Rh antigen associated with acquired Rh antibodies and a chromosome translocation in a patient with myeloid metaplasia B Cooper, PV Tishler, L Atkins and WR Breg Myeloid metaplasia is a clonal disease of the marrow pluripotent stem cell in which a constant cytogenetic abnormality could result in an altered antigenic characteristic of hematopoietic cells. A 57-yr-old man who had acquired myeloid metaplasia at age 37 was noted to be Rh negative, although blood typing at age 33 was Rh positive. His erythrocytes reacted with anti-c and anti-e, typical for an Rh negative individual. Analysis of 11 metaphase bone marrow cells by G-banding revealed 46 chromosomes with a consistent anomaly in 100% of cells involving chromosomes 1 and 13. The changes were consistent with a reciprocal translocation, with break points at approximately 1p32 and 13q22, although break points at 1p13 and 13q14 were also possible. Since previous cytogenetic data have localized the Rh gene to the short arm of chromosome 1, our data indicate the Rh gene lies within the segment u13 leads to 1p32. Serum of this patient had circulating anti-D and anti-C antibodies. Consequently, this patient lost immunologic tolerance to a "self antigen" after losing the ability to express this antigen. Volume 54, Issue 3, pp. 642-647, 09/01/1979 Copyright © 1979 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: G. F. Kormoczi, E.-M. Dauber, O. A. Haas, T. J. Legler, F. B. Clausen, G. Fritsch, M. Raderer, C. Buchta, A. L. Petzer, D. Schonitzer, et al. Mosaicism due to myeloid lineage restricted loss of heterozygosity as cause of spontaneous Rh phenotype splitting Blood, September 15, 2007; 110(6): 2148 - 2157. [Abstract] [Full Text] [PDF]

	Copyright © 1979 by American Society of Hematology         Online ISSN: 1528-0020