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Oncogenes and tumor suppressor genes
1Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Abstract:
The artificial selection of the directly acting or acute RNA tumor viruses for high transforming ability has led to the isolation of defective retroviral genomes that have picked up, by accidental recombination, some of the important genes that influence, trigger or regulate cell division. These genes belong to at least four functionally different groups. Each of them can contribute to tumor development and/or progression after activation by structural or regulatory changes. Growth factor genes may act as oncogenes following constitutive activation in a cell that normally responds to, but does not produce, the corresponding growth factor (the autocrine model, exemplified by sis). Growth factor receptors may be fixed in a state of continuous, faulty signalling by the truncation of their external, ligand binding portion (examples: erb-B, fms). Genes coding for proteins involved in signal transduction may be activated by point mutations in certain, important domains (example: the ras-family). DNA binding proteins, presumably involved in DNA replication may drive cell division after constitutive activation by retroviral insertion, chromosomal translocation or gene amplification (example: the myc-family).
Insights
Retroviruses carrying oncogenes can cause cancer by altering cell division genes. These oncogenes, including growth factors and receptors, drive tumor development through various genetic changes.
Area of Science:
- Oncology
- Molecular Biology
- Virology
Background:
- Artificial selection of RNA tumor viruses yields defective retroviral genomes.
- These genomes acquire host genes influencing cell division via recombination.
Purpose of the Study:
- To identify and categorize genes that, when altered by retroviruses, contribute to cancer.
- To understand the mechanisms by which these genes promote tumor development and progression.
Main Methods:
- Analysis of retroviral genomes isolated after artificial selection for high transforming ability.
- Identification of acquired host genes involved in cell division regulation.
Main Results:
- Four functional groups of cell division genes are implicated in oncogenesis.
- Mechanisms include autocrine growth factor signaling (sis), truncated growth factor receptors (erb-B, fms), mutated signal transduction proteins (ras-family), and activated DNA-binding proteins (myc-family).
Conclusions:
- Acquisition and activation of host cell division genes by retroviruses are key mechanisms in viral oncogenesis.
- Specific gene families (growth factors, receptors, signal transducers, DNA-binding proteins) play critical roles in tumor initiation and progression.