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Related Experiment Videos

Oncogene mobility in a human leukemia line HL-60.

S R Wolman, L Lanfrancone, R Dalla-Favera

    Cancer Genetics and Cytogenetics
    |June 1, 1985
    PubMed
    Summary

    This study maps amplified c-myc oncogene DNA in HL-60 leukemia cells. Amplified c-myc DNA localizes to a marker chromosome, M3q+, and an 8q+ chromosome, revealing new insights into cancer gene behavior.

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    Area of Science:

    • Human genetics
    • Cancer biology
    • Molecular cytogenetics

    Background:

    • HL-60 cells, derived from human promyelocytic leukemia, exhibit c-myc oncogene amplification.
    • Reported chromosomal aberrations in HL-60 include double minutes (DMs) and an abnormally banded region (ABR) on chromosome 8.
    • A link between these aberrations and c-myc DNA amplification has been hypothesized.

    Purpose of the Study:

    • To localize amplified c-myc DNA within HL-60 cells using cytologic hybridization.
    • To investigate the chromosomal integration sites of amplified c-myc.
    • To understand the chromosomal mechanisms underlying c-myc amplification in leukemia.

    Main Methods:

    • Cytologic hybridization was employed to determine the location of amplified c-myc DNA.

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  • Analysis was performed on early passage HL-60 cells and later passage clones.
  • Karyotyping and chromosome banding techniques were utilized to identify chromosomal abnormalities.

    • Main Results:

    • Amplified c-myc DNA was localized to a marker chromosome, M3q+, in early passage HL-60 cells.
    • In later passage clones, c-myc was found at an ABR on an 8q+ chromosome.
    • The M3q+ chromosome likely resulted from a translocation t(5p;17q) with c-myc amplification material inserted into 17q.

    Conclusions:

    • Amplification and chromosomal integration of c-myc can occur at sites distinct from its native locus.
    • Different integration sites for amplified c-myc can be observed in different lineages of the same tumor.
    • These findings provide insights into the dynamic nature of oncogene amplification in cancer development and progression.