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Using retroviruses as insertional mutagens to identify cellular oncogenes.

Progress in Clinical and Biological Research

|January 1, 1983

Summary

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.

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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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