Abstract
It is estimated that 15% of all cancers are etiologically linked to viral infection. Specific cancers including adult T-cell leukemia, hepatocellular carcinoma, and uterine cervical cancer are associated with infection by human T-cell leukemia virus type I, hepatitis B virus, and high-risk human papilloma virus, respectively. In these cancers, genomic instability, a hallmark of multistep cancers, has been explicitly linked to the expression of oncoproteins encoded by these viruses. This review discusses mechanisms utilized by these viral oncoproteins, Tax, HBx, and E6/E7, to mediate genomic instability and cellular transformation.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Cell Cycle / physiology
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism*
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DNA Repair / genetics
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Genomic Instability*
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Hepatitis B virus / genetics
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Hepatitis B virus / metabolism
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Human T-lymphotropic virus 1 / genetics
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Human T-lymphotropic virus 1 / metabolism
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Humans
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Models, Biological
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Neoplasms / etiology*
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Neoplasms / metabolism
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Neoplasms / virology
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Oncogene Proteins / metabolism*
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Oncogenic Viruses / genetics
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Oncogenic Viruses / metabolism*
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Papillomaviridae / genetics
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Papillomaviridae / metabolism
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Transcription, Genetic / genetics*
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Tumor Suppressor Proteins / metabolism
Substances
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Oncogene Proteins
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Tumor Suppressor Proteins