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Published on: December 4, 2007

Using retroviruses as insertional mutagens to identify cellular oncogenes

H E Varmus

    Progress in Clinical and Biological Research
    |January 1, 1983
    PubMed

    Insights

    Retroviruses can activate cellular oncogenes through insertional mutagenesis, leading to cancer. Studies show viral DNA insertions near specific genes like c-myc can drive tumor formation in various animal models.

    Area of Science:

    • Molecular Biology
    • Oncology
    • Virology

    Background:

    • Cellular genes implicated in oncogenesis are identified by homology to viral oncogenes, altered expression in tumors, or transforming activity.
    • Retroviruses lacking oncogenes may activate cellular oncogenes via insertional mutagenesis.

    Purpose of the Study:

    • To investigate the hypothesis that retroviruses activate cellular oncogenes through insertional mutagenesis.
    • To identify activated cellular genes in tumor cells by locating proviral insertions in flanking DNA.

    Main Methods:

    • Locating proviruses in the chromosomal DNA of tumor cell populations.
    • Identifying activated transcriptional units in cellular DNA adjacent to proviral insertions.

    Main Results:

    • Avian leukosis virus (ALV) DNA insertion activates the c-myc gene.
    • Mouse mammary tumor virus (MMTV) proviruses are found in a specific genomic region in mammary carcinomas.
    • Proviruses of ALV, chicken syncytial virus (CSV), and myeloblastosis-associated virus (MAV) target the c-myc locus in avian B cell lymphomas.
    • MAV-induced nephroblastomas lack proviral insertions near c-myc, indicating gene-specific viral activity.

    Conclusions:

    • Insertional mutagenesis by retroviruses is a mechanism for oncogene activation.
    • The c-myc gene is a common target for viral oncogenesis.
    • Different viruses can activate the same oncogene, and the same virus can activate different oncogenes depending on the tumor type.

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