Viruses associated with human cancer.
It is estimated that viral infections contribute to 15-20% of all human cancers. As obligatory intracellular parasites, viruses encode proteins that reprogram host cellular signaling pathways that control proliferation, differentiation, cell death, genomic integrity, and recognition by the immune system. These cellular processes are governed by complex and redundant regulatory networks and are surveyed by sentinel mechanisms that ensure that aberrant cells are removed from the proliferative pool. Given that the genome size of a virus is highly restricted to ensure packaging within an infectious structure, viruses must target cellular regulatory nodes with limited redundancy and need to inactivate surveillance mechanisms that would normally recognize and extinguish such abnormal cells. In many cases, key proteins in these same regulatory networks are subject to mutation in non-virally associated diseases and cancers. Oncogenic viruses have thus served as important experimental models to identify and molecularly investigate such cellular networks. These include the discovery of oncogenes and tumor suppressors, identification of regulatory networks that are critical for maintenance of genomic integrity, and processes that govern immune surveillance.
McLaughlin-Drubin
Margaret E
ME
The Channing Laboratory, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, 8th Floor, 181 Longwood Avenue, Boston, MA 02115, USA. mdrubin@rics.bwh.harvard.edu
Munger
Karl
K
D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D042822:Genomic Instability; D006801:Humans; D007157:Immunologic Surveillance; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics / Q000821:virology*; D009858:Oncogenic Viruses / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics; D014412:Tumor Virus Infections / Q000235:genetics