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Insertional oncogenesis by non-acute retroviruses: implications for gene therapy
1Department of Molecular Biology and Biochemistry, Cancer Research Institute, University of California, Irvine, CA 92697, USA. hyfan@uci.edu
Viruses
|October 14, 2011
Summary
Non-acute retroviruses cause cancer by integrating viral DNA into host cells, activating proto-oncogenes. This review details insertional activation mechanisms and proto-oncogene discovery, crucial for understanding oncogenesis and gene therapy risks.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Retroviruses are known to cause cancers in humans and animals.
- Research has illuminated oncogenesis mechanisms, including viral and cellular proto-oncogenes.
- Non-acute retroviruses, lacking oncogenes, induce tumors through insertional activation of proto-oncogenes.
Purpose of the Study:
- To review the mechanisms by which non-acute retroviruses cause cancer.
- To highlight the role of insertional activation of cellular proto-oncogenes.
- To discuss the discovery of proto-oncogenes and their cooperation in tumorigenesis.
Main Methods:
- Review of early research on insertional activation in virus-induced tumors.
- Identification of common insertion sites (CISs) to discover new proto-oncogenes.
- Retroviral tagging in susceptible mice to identify active proto-oncogenes in oncogenic pathways.
- Utilizing technical advances like PCR cloning, mouse genome sequence, and high-throughput sequencing.
Main Results:
- Insertional activation of proto-oncogenes by viral DNA integration is a key mechanism.
- Discovery of novel proto-oncogenes through CIS analysis.
- Elucidation of proto-oncogene cooperation in tumor development.
- Identification of cellular proto-oncogenes involved in specific oncogenic pathways.
Conclusions:
- Non-acute retroviral oncogenesis is primarily driven by insertional activation of proto-oncogenes.
- Studies have significantly advanced the discovery of proto-oncogenes and understanding of oncogenic pathways.
- Insertional activation poses risks in gene therapy using retroviral vectors, necessitating careful consideration of oncogenesis mechanisms.
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