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Prepublished online as a Blood First Edition Paper on June 19, 2003; DOI 10.1182/blood-2003-01-0031. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-01-0031v1 102/7/2597    most recent 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 Wang, L. Articles by Hirai, H. Search for Related Content PubMed PubMed Citation Articles by Wang, L. Articles by Hirai, H. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2003, Vol. 102, No. 7, pp. 2597-2604 NEOPLASIA Molecular characterization of the recurrent unbalanced translocation der(1;7)(q10;p10) Lili Wang, Seishi Ogawa, Akira Hangaishi, Ying Qiao, Noriko Hosoya, Yasuhito Nanya, Kazuma Ohyashiki, Hideaki Mizoguchi, and Hisamaru Hirai From the Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Japan; the First Department of Internal Medicine, Tokyo Medical University, Japan; and the Department of Hematology, Tokyo Women's Medical University, Japan. An unbalanced translocation der(1;7)(q10; p10) is a nonrandom chromosomal aberration commonly observed in myelodysplastic syndrome and acute myeloid leukemia. We molecularly analyzed the breakpoints of der(1;7)(q10;p10) by quantitative fluorescent in situ hybridization (FISH) analyses using centromeric satellite DNAs mapped to chromosomes 1 and 7 as probes. We found that the signal intensities of 2 centromere alphoid probes, D1Z7 on chromosome 1 and D7Z1 on chromosome 7, were almost invariably reduced on the derivative chromosome compared with those on their normal counterparts. These results suggest that this translocation results from the recombination between the 2 alphoids, which was further confirmed by fiber FISH experiments. Because the relative reduction in the intensities of D1Z7 and D7Z1 signals on the derivative chromosomes was highly variable among patients, it was estimated that the breakpoints in these patients were randomly distributed over several megabase pairs within each alphoid cluster except for its extreme end to the short arm. Our results provide a novel insight into the structural basis for generation of this translocation as well as its leukemogenic roles. (Blood. 2003;102:2597-2604) 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]

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