Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation.
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.
Gatza
Michael L
ML
Interdepartmental Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Chandhasin
Chandtip
C
Ducu
Razvan I
RI
Marriott
Susan J
SJ
D002453:Cell Cycle / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism*; D004260:DNA Repair / Q000235:genetics; D042822:Genomic Instability; D006515:Hepatitis B virus / Q000235:genetics / Q000378:metabolism; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000378:metabolism / Q000821:virology; D015513:Oncogene Proteins / Q000378:metabolism*; D009858:Oncogenic Viruses / Q000235:genetics / Q000378:metabolism*; D027383:Papillomaviridae / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000378:metabolism
D015513:Oncogene Proteins; D025521:Tumor Suppressor Proteins