The use of gene transfer and recombinant DNA techniques has made it possible to identify a number of oncogenes that are active in human tumors and are presumably responsible for the altered properties of the tumor cells. Workers have identified a large number of these cellular oncogenes as well as oncogenes of viral origin. A main goal of the proposed work is to understand how the actions of these various oncogenes may be integrated into a scheme that describes the growth regulatory networks of the cell. Some of these oncogenes have been found to collaborate with others in tumorigenic conversion of cells. This has allowed a classification of some into a functional group characterized by having properties similar to the ras oncogenes. The paradigm of the second group is the myc oncogene. Proposed work will undertake to analyze the nature of other oncogenes. A second scheme by which oncogenes may be understood stems from the principle that these genes confer on the cell an autonomy from normally required growth factors. Such oncogenes may provide the cell with its own growth factors. Proposed experiments will investigate whether a growth factor gene can be activated into an oncogene. Alternatively, growth factor autonomy may be achieved by alterations in a cellular growth factor receptor. Proposed experiments will examine an oncogene protein that appears to function as a growth factor receptor. Other experiments will study ras p21 proteins that may transmit growth stimuatory signals sent out by the receptors. Longer term experiments will examine tumor genes that enable cells to metastasize or escape immune surveillance.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Unknown (R35)
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Special Emphasis Panel (SRC (88))
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Whitehead Institute for Biomedical Research
United States
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