Oncogenes are essentially dominant growth enhancing genes and if overexpressed can augment growth in one cell type but impede growth or stimulate programmed cell death in another cell type. The phenomenon of oncogene addiction describes cancer cell dependence on individual oncogenes to sustain the malignant phenotype. Oncogenic functions are activated by them. Cancer cell survival relies on quite a few key genetic driver events. When an oncogene is turned off this means that the cancer cells will undergo programmed cell death. For instance, in transgenic mice when there is the expression of an inducible form of the H-ras oncogene it develops melanomas. When the ras gene was switched off apoptosis occurred and regressed. Another instance is with the expression of a Bcr-Abl fusion gene which results in the development of leukemia and killed mice. When switched off, even at advanced stages of disease, the leukemic cells underwent rapid apoptosis and this resulted in mice surviving. In cancer cells the regulation of signal transduction and gene expression is rather crazy and distinct of normal cells. Since they have a different form of regulation it is said that cancer cells may be more reliant on the activity of specific oncogenes. In addition, they are more sensitive to the growth-inhibitory effects of specific tumor suppressor genes like p53 versus normal cells.
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