OverviewBishop begins his lecture with a historical review of the experiments that resulted in the realization that cancer has a genetic basis. He explains that mutations can cause normal cellular genes known as proto-oncogenes to become oncogenes, analogous to jammed accelerators causing uncontrolled cell division. Alternatively, mutations in tumor suppressor genes are analogous to a failed brake system. An accumulation of both types of mutation leads to the development of cancer. In part 2 of his lecture, Bishop describes how the sequencing of cancer genomes will advance the study and management of cancer on various fronts, including the discovery of causes, the improvement of early detection, the prediction of outcome and the development of new therapeutics. He stresses the promise of designing therapeutics that can be targeted to those patients most likely to benefit from these drugs. Bishop expands on this theme in part 3 where he describes experiments to find drugs that exploit vulnerabilities created by cancer genes, utilizing a genetic strategy known as “synthetic lethality.” |
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