Viral oncogenesis and cell cycle control.
Increasing evidence suggests a critical role for cell cycle regulatory genes in tumorigenesis in mammals, and oncogenic viruses account for a considerable proportion of cancers in humans. In most cases, infection by oncogenic viruses is insufficient for malignant transformation; rather, the viruses provide host cells with additional growth stimuli, which extend the proliferative capacity of the infected cell. This implies that viral oncogenes can override cellular control mechanisms, which in untransformed cells regulate cell cycle progression in response to various antiproliferative signals. Recent progress has enabled the definition of several mammalian cell cycle regulatory genes as targets for viral oncoproteins. This new field of investigation was the central topic of a meeting (Viral Oncogenesis and Cell Cycle Control) held in Heidelberg in October 1995. In the following, major findings presented at this meeting will be summarized. The first part of the meeting was dedicated to the analysis of cell cycle regulation in normal untransformed mammalian cells, followed by an analysis of the interaction of tumor virus oncoproteins with mammalian cell cycle regulators. The latter interactions fall into three categories: viral oncoproteins were shown to interfere with various signal transduction pathways, to inactivate growth-suppressive nuclear proteins by direct binding, and to modulate the expression of key cell cycle regulatory genes.
Jansen-Dürr
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Deutsches Krebsforschungszentrum, Forschungsschwerpunkt, Angewandte Tumorvirologie, Heidelberg, Germany.
D000818:Animals; D002453:Cell Cycle; D015870:Gene Expression; D008322:Mammals; D009687:Nuclear Proteins / Q000378:metabolism; D015513:Oncogene Proteins / Q000378:metabolism; D011991:Receptors, Virus / Q000378:metabolism; D015398:Signal Transduction; D014780:Viruses / Q000235:genetics / Q000378:metabolism*
D009687:Nuclear Proteins; D015513:Oncogene Proteins; D011991:Receptors, Virus