SEARCH:   Advanced

This Article Full Text (PDF) 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 Fitzgerald, T. J. Articles by Goorha, R. M. Search for Related Content PubMed PubMed Citation Articles by Fitzgerald, T. J. Articles by Goorha, R. M. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Rhom-2 expression does not always correlate with abnormalities on chromosome 11 at band p13 in T-cell acute lymphoblastic leukemia TJ Fitzgerald, GA Neale, SC Raimondi and RM Goorha Department of Virology and Molecular Biology, St Jude Children's Research Hospital, Memphis, TN 38101. A frequent site for nonrandom recombination in T-cell acute lymphoblastic leukemia (T-ALL) is chromosome 11 at p13. The molecular characterization of a (7;11)(q35;p13) translocation showed that the translocation breakpoint was 2 kb 5' to the T-ALLbcr locus resulting in the juxtaposition of the T-cell receptor (TCR) beta gene to the rhom-2 gene locus. Northern blot analysis did not detect expression of the rhom-2 gene in the leukemic blasts of the (7;11) translocation. However, using a sensitive polymerase chain reaction (PCR)-based assay, the (7;11) translocation showed a trace expression of rhom-2 at a level of 0.01% of TCR-beta message. Because rhom-2 is considered a proto- oncogene, the significance of the trace expression of rhom-2 in the (7;11) translocation was investigated by comparing the level of rhom-2 expression in 7 additional T-ALLs, normal thymocytes, and CEM (pre-T) and HPB (mature-T) cell lines using the PCR assay. The CEM cells, normal thymocytes, and one patient, whose blasts had no cytogenetic abnormality of chromosome 11, did not express rhom-2 indicating that rhom-2 is not normally expressed in T cells. The other six T-ALLs fell into three categories: (1) two T-ALLs overexpressed rhom-2 in the presence of a translocation; (2) two T-ALLs had trace expression in the presence of a translocation; and (3) two T-ALLs had trace expression with no observable abnormalities on chromosome 11 at p13. Therefore, the data indicate that not all translocations at the T-ALLbcr locus result in overexpression of rhom-2. To account for the sharp contrast in rhom-2 expression seen in these T-ALLs, a model is proposed with a negative regulatory element in the T-ALLbcr locus that is disrupted in some of the cases leading to overexpression of rhom-2. Volume 80, Issue 12, pp. 3189-3197, 12/15/1992 Copyright © 1992 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: W. A. Dik, B. Nadel, G. K. Przybylski, V. Asnafi, P. Grabarczyk, J. M. Navarro, B. Verhaaf, C. A. Schmidt, E. A. Macintyre, J. J. M. van Dongen, et al. Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL Blood, July 1, 2007; 110(1): 388 - 392. [Abstract] [Full Text] [PDF] J.-R. Landry, S. Kinston, K. Knezevic, I. J. Donaldson, A. R. Green, and B. Gottgens Fli1, Elf1, and Ets1 regulate the proximal promoter of the LMO2 gene in endothelial cells Blood, October 15, 2005; 106(8): 2680 - 2687. [Abstract] [Full Text] [PDF]

	Copyright © 1992 by American Society of Hematology         Online ISSN: 1528-0020