For this purpose, we used the MMTV-PyMT murine model whose oncogenesis is induced by expression of the polyoma virus middle T oncoprotein under control of the Mouse Mammary Tumour Virus (MMTV) promoter (PMID: 1312220).
Furthermore, abnormal centrosome function can be induced by expression of the papilloma virus genes E6 and E7, inhibiting normal TP53 and RB1 activity, respectively (Duensing et al, 2000).
This has been extended to (Mφ-derived) anti-inflammatory cytokines (that is, IL-4, IL-10, IL-13, IFN-β, or TGF-β) and to 'molecular synovectomy' (either by expression of herpes simplex virus-thymidine kinase with subsequent administration of ganciclovir or by overexpression of Fas-ligand/inhibitors of nuclear translocation of NF-κB, resulting in synovial cell apoptosis [ 88, 91, 92]).
It is confirmed by expression of viral NS3 antigen and virus plaque-forming units.
Reversibility of salivary oncogenesis initiated by expression of the complex oncoprotein Large Simian Virus 40 T antigen, which disrupts both pRB-related and p53 tumor suppressor pathways, is interrupted at a preneoplastic stage in a time-dependent manner [ 11].
Virus infection as detected by expression of the E2 viral glycoprotein was significantly reduced in SK2 knockdown-infected cells.
Virus-like particles (VLPs) were produced by expression of an HPV-16 L1 recombinant baculovirus in insect cells.
Transgenic mouse models characterized by conditional expression of the simian virus 40 T antigen oncogene in postmitotic neurons clearly presented a neurodegenerative phenotype, consequence of forced cell cycle activation [ 32].
They convincingly demonstrated that deletion of MET in neutrophils was associated with increased tumor growth and metastasis in multiple tumor models in mice, including spontaneous mammary tumors driven by transgenic expression of the polyoma virus middle T (PyMT) antigen.
In a mouse model of mammary tumors initiated by the expression of the polyoma virus middle T oncoprotein, the null mutation in the colony-stimulating factor-1 gene CSF-1 to deplete macrophages has been demonstrated to reduce the progression of preinvasive lesions to malignant lesions and attenuate the formation of lung metastasis [ 7].
