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Related Experiment Videos

A translocated human c-myc oncogene is altered in a conserved coding sequence.

W Murphy, J Sarid, R Taub

    Proceedings of the National Academy of Sciences of the United States of America
    |May 1, 1986
    PubMed
    Summary
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    Researchers cloned and characterized the MYC oncogene in Burkitt lymphoma, finding it translocated and altered. Despite mutations, the MYC oncogene retained reduced transforming ability.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Genetics

    Background:

    • Burkitt lymphoma is associated with chromosomal translocations involving the MYC oncogene.
    • The immunoglobulin heavy chain locus, specifically the mu switch region, is a common site for MYC translocation.
    • Understanding these translocations is crucial for deciphering oncogenesis.

    Purpose of the Study:

    • To clone and characterize the MYC oncogene translocated in a Burkitt lymphoma cell line.
    • To investigate the molecular consequences of MYC translocation on gene expression and protein structure.
    • To assess the functional impact of the altered MYC oncogene.

    Main Methods:

    • Gene cloning and characterization techniques.
    • Analysis of translocation breakpoints within the MYC gene and immunoglobulin locus.

    Related Experiment Videos

  • Transcriptional analysis to identify novel promoter usage.
  • Protein sequence analysis to detect mutations.
  • Functional assays (e.g., focus-formation assay) to evaluate transforming ability.

    • Main Results:

    • Successfully cloned and characterized the translocated MYC oncogene.
    • Identified the translocation breakpoint within the first intron of MYC, separating coding exons.
    • Discovered transcription initiated from a cryptic intronic promoter, resulting in an altered 5' untranslated region.
    • Observed significant alterations in the MYC protein sequence due to frameshift mutations in a conserved region.
    • Demonstrated that the mutated MYC oncogene retains a reduced transforming ability.

    Conclusions:

    • The translocation in Burkitt lymphoma leads to a novel transcriptional start site and altered MYC protein.
    • Despite substantial molecular changes, the MYC oncogene retains partial transforming capacity.
    • These findings contribute to understanding the complex mechanisms of MYC dysregulation in cancer.