The Theory Of Oncogenes

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Oncogenes, also known as “cancer promoting genes”, are specific genes whose mutations can lead to the excessive proliferation of cells and lead to the development of cancer. These genes are divided into classes based on their “cancer-promoting” abilities (Alberts 2007). Proto-oncogenes are the first gene class. They cause a “gain-of function mutation” which can lead a cell to a proliferative cancer form (Alberts 2007). The resulting mutant, which is then “overactive or overexpressed” is the oncogenic form (Alberts 2007). The second class of these genes are ones that cause a “loss-of-function mutation”. These are tumor suppressor genes, which can also lead to cancer. Both of these gene classes have similarities in the ways in which they contribute to cancer proliferation, and are therefore considered to be “flip sides of the same coin” (Alberts 2007).
One of the recent developments in the research behind oncogenesis and its relationship to cancer is the theory of “oncogenic addiction”. This theory explains the phenomena of “a tumor cell seemingly exhibiting dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “switch off the crucial pathway of dependence”, which in theory should negatively affect or inhibit the cancer, “while sparing normal cells that are not similarly addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and see that there is toleration without “obvious consequences” (Sharma & Settleman 2007). This is the concept of “addiction” in cancer, and the dependence on particular genes to activate prolifer...

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...need to be developed to begin this study, we can infer from past research the steps in which determination of these relationships could be done. After developing a line in which a proper analysis can be done, where the phosphorylation of Src can be analyzed, western blotting would be the first major step in this experiment (Pillay et al. 2009). The Western blot would be used here to determine the levels of Src-kinase and phosphorylated Src-kinase in the cancer cells (Pillay et al. 2009). The lysates from the cells would be immunoprecipitated and analyzed for these levels as well as the levels of EGFR in the cells (Pillay et al. 2009). After the samples are transferred to the proper membrane, a designed monoclonal antibody (mAb) would be used to probe for the phosphorylated Src-kinase. Similarly a mAb would be used for probing the attached EGFR (Pillay et al. 2009).
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