Molecular mechanisms of virus-induced carcinogenesis: the interaction of viral factors with cellular tumor suppressor proteins.
Accumulating evidence indicates that tumor viruses represent a major etiological factor in a significant portion of human cancers. These cancers include human papillomavirus induced anogenital cancers, hepatitis B and C virus associated hepatocellular carcinomas, nasopharyngeal carcinomas and lymphomas linked to Epstein-Barr virus infection, and human T cell leukemia virus associated adult T cell leukemias. This review summarizes the recent progress made in understanding the molecular mechanisms of viral carcinogenesis, with a particular focus on the interaction of viral factors with cellular tumor suppressor proteins. The functional inactivation of tumor suppressor proteins may represent a common strategy by which several tumor viruses contribute to malignant cell transformation.
Hoppe-Seyler
F
F
Angewandte Tumorvirologie, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
Butz
K
K
D002453:Cell Cycle; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004268:DNA-Binding Proteins / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D006801:Humans; D009369:Neoplasms / Q000821:virology*; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D009857:Oncogenes; D009858:Oncogenic Viruses / Q000235:genetics / Q000502:physiology*; D016160:Retinoblastoma Protein / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D004268:DNA-Binding Proteins; D009856:Oncogene Proteins, Viral; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53