Compare and Contrast Tumor Suppressor Genes and Proto-Oncogenes

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Compare and contrast tumour suppressor genes and proto-oncogenes. Discuss an example of how recent advances in our understanding of these genes have led to the development of a novel therapy that is being used in the treatment of human cancer.
Cancer known in medicine as a malignant neoplasm is one of the biggest killers worldwide. In 2007, cancer caused roughly 13% (7.9 million) of the planet’s deaths (Jemal, 2011). This will more greatly affect an aging society such as ours in years to come, and yet it is already the foremost cause of death in the developed world. The main reason cancer causes so many fatalities the body’s inability to mount an effective response to the failure of DNA replication within the body. This results in a mass
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Mutations (for most cancers) must appear in both tumour suppressing genes and oncogenes for cancers to form. The tumour suppressing genes and oncogenes act in complementary fashion to one another; one pulls forward, and the other pushes back ensuring that the cell cycle occurs in a controlled manner (Sherr, 2004).
Oncogenes were discovered in the 1960s, when it was discovered that some animal cancers such as lymphomas were caused by viruses. Some of these viruses were notable due to the simplicity of their RNA genome. These viruses only had three distinct transcription units, involved in the replication of the virus (coat proteins and reverse transcriptase etc.), and an extra gene. This was an oncogene. When oncogenes are properly functioning they are termed proto-oncogenes (Todd R, 1999). Their normal function is to control cell proliferation. These function in growth signalling pathways, and conversely to tumour suppressing cells are activated through a gain in function rather than a loss of it. This occurs in two ways, by producing more of a product, or producing a subtly different product, as a result of a mutation similar to tumour suppressor genes (Croce, 2008). Oncogenes play a particularly strong role in the development of breast cancers. Often the normal ERBB2 and other related genes are amplified in late stage neuroblastomas and rhabdomyosarcomas. ERBB2 encodes HER2 which is a member of the epidermal growth factor

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