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    Cytogenetic and Genome Research
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    1986
    This article was originally published in
    Cytogenetics and Cell Genetics
    Issue Cover
    Research Articles|May 08 2008

    Sublocalization ofc-myb to 6q21→q23 by in situ hybridization andc-myb expression in a human teratocarcinoma with 6q rearrangements

    Subject Area:Genetics
    J.W.G. Janssen;
    J.W.G. Janssen
    aDivisions of Cell Biology and Molecular Biology, The Netherlands Cancer Institute, Amsterdam, and
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    P. Vernole;
    P. Vernole
    aDivisions of Cell Biology and Molecular Biology, The Netherlands Cancer Institute, Amsterdam, and
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    P.A.J. de Boer;
    P.A.J. de Boer
    aDivisions of Cell Biology and Molecular Biology, The Netherlands Cancer Institute, Amsterdam, and
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    J.W. Oosterhuis;
    J.W. Oosterhuis
    bDepartment of Pathology, University of Groningen, Groningen
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    J.G. Collard
    J.G. Collard
    aDivisions of Cell Biology and Molecular Biology, The Netherlands Cancer Institute, Amsterdam, and
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    Cytogenetics and Cell Genetics (1986) 41 (3): 129–135.
    Article history
    Accepted:
    August 21 1985
    Published Online:
    May 08 2008
    Citation

    J.W.G. Janssen,P. Vernole,P.A.J. de Boer,J.W. Oosterhuis,J.G. Collard; Sublocalization ofc-myb to 6q21→q23 by in situ hybridization andc-myb expression in a human teratocarcinoma with 6q rearrangements.Cytogenetics and Cell Genetics 1 March 1986; 41 (3): 129–135.https://doi.org/10.1159/000132217

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      Abstract

      We have sublocalized the human proto-oncogenec-myb by applying two different techniques: in situ hybridization of metaphase spreads and chromosome spot hybridization of flow-sorted chromosomes. For this we used a teratocarcinoma cell line carrying specific chromosome translocations involving the two chromosomes 6 and one chromosome 11. The distribution of thec-myb gene copies on the different translocation chromosomes revealed thatc-myb is located in the region 6q21→q23. Because of the close proximity of thec-myb locus to the chromosomal breakpoints in the teratocarcinoma, we investigated whetherc-myb was implicated in the development of this tumor. No rearrangement, deletion, or amplification of the gene was detected in the teratocarcinoma cells. Furthermore, the level ofc-myb expression was comparable to that of other cell lines of nonhematopoietic origin. These results suggest thatc-myb was not affected by the translocation and played no significant role in the development of this teratocarcinoma.

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      © 1986 S. Karger AG, Basel
      1986
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