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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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Fioretos, T Articles by Groffen, J Search for Related Content PubMed PubMed Citation Articles by Fioretos, T Articles by Groffen, J Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  No evidence for genomic imprinting of the human BCR gene T Fioretos, N Heisterkamp and J Groffen Department of Pathology, Childrens Hospital of Los Angeles, CA 90027. Chronic myeloid leukemias and 5% to 20% of acute lymphoid leukemias are characterized by the Philadelphia chromosome, a reciprocal chromosomal translocation, t(9;22)(q34;q11), generating BCR-ABL and ABL-BCR fusion genes. Cytogenetic studies have recently shown a preferential involvement of the paternally derived chromosome 9 and the maternally derived chromosome 22 in this translocation, indicating that imprinting might be involved in the formation or selection of the translocation. In this study, we have identified a BamHI polymorphism in the coding region of BCR exon 1, allowing us to investigate whether both BCR alleles are transcribed. By using a reverse transcriptase-polymerase chain reaction assay, we show that both BCR alleles are expressed in the peripheral blood cells of normal individuals. Volume 83, Issue 12, pp. 3441-3444, 06/15/1994 Copyright © 1994 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

	Copyright © 1994 by American Society of Hematology         Online ISSN: 1528-0020