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1 event between a replicating retrovirus and a cellular oncogene.
2 12 region that can be co-amplified with this cellular oncogene.
3 increased proliferation and upregulation of cellular oncogenes.
4 mbers of this family have been identified as cellular oncogenes.
5 ctory to transformation by several viral and cellular oncogenes.
6 formation in cooperation with other viral or cellular oncogenes.
7 endoplasmic reticulum (ER) stress caused by cellular oncogene activation and a hostile tumor microen
8 ing CRISPR screens, we previously identified cellular oncogene addictions in PEL cell lines, includin
10 have suggested that upregulation of various cellular oncogenes and cytokines by Tax may explain the
11 integrating into the host genome, activating cellular oncogenes and microRNAs, or inactivating tumor
13 fic expression of MMTV and the activation of cellular oncogenes are located within two enhancer eleme
15 etal bovine serum or exogenous expression of cellular oncogene Bcl-xL prevented CG-4 cells from MHV-i
17 on pathways by mutation or overexpression of cellular oncogenes has been associated with neoplastic t
20 for transformation by a variety of viral and cellular oncogenes in a mouse embryo fibroblast model.
21 iated by viral proteins in the activation of cellular oncogenes, inactivation of tumor-suppressor gen
24 transmembrane receptor encoded by the HER-2 cellular oncogene is amplified in several types of human
26 show that the extent of ER stress induced by cellular oncogenes may define the mechanism of activatio
27 -proliferation and transformation, viral and cellular oncogenes need to circumvent DDR-induced cell-c
28 ependently of the presence of other viral or cellular oncogenes, or of whether the cells are long-ter
29 tumors by insertion of viral DNA adjacent to cellular oncogenes, resulting in altered expression and/
30 oned rat embryo fibroblast (CREF) cells with cellular oncogenes results in acquisition of anchorage-i
32 trate a collaborative relationship between 2 cellular oncogenes that also contribute to cell fate det
33 E1A gene, that may exploit the activity of a cellular oncogene, the c-MYC gene, in addition to inacti