Compare and Contrast Tumor Suppressor Genes and Proto-Oncogenes
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 of uncontrolled tissue proliferation which eventually leads to death. Approximately, 50% of all people who get cancer will eventually succumb to the disease (Jemal, 2011). It is therefore essential that new methods for controlling the disease are found to improve the prognosis of suffers.
Tumour suppressor genes normally function to uncontrolled proliferation of cells within the body. They do this through a variety of means, they might prevent inappropriate progression of the cell cycle, or drive already cancerous cells towards apoptosis, and others simply check for errors during replication increasing fidelity (Sherr, 2004). Mutant versions that are present in cancers have lost the function to perform any of these properly. In contrast to oncogenes, tumour suppressor cells generally follow the two hit hypothesis (Knudson, 2001). The hypothesis indicates that two mutations must affect both of the normally dominant tumour suppressor cells before a mutant phenotype is seen. Proto-Oncogenes are usually recessive, hence it only takes a single mutation to one of the alleles (to become dominant as it is a gain of function mutation) before a mutant phenotype is seen. Although, this is not true for all cancers, and sometimes the tumour
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 of uncontrolled tissue proliferation which eventually leads to death. Approximately, 50% of all people who get cancer will eventually succumb to the disease (Jemal, 2011). It is therefore essential that new methods for controlling the disease are found to improve the prognosis of suffers.
Tumour suppressor genes normally function to uncontrolled proliferation of cells within the body. They do this through a variety of means, they might prevent inappropriate progression of the cell cycle, or drive already cancerous cells towards apoptosis, and others simply check for errors during replication increasing fidelity (Sherr, 2004). Mutant versions that are present in cancers have lost the function to perform any of these properly. In contrast to oncogenes, tumour suppressor cells generally follow the two hit hypothesis (Knudson, 2001). The hypothesis indicates that two mutations must affect both of the normally dominant tumour suppressor cells before a mutant phenotype is seen. Proto-Oncogenes are usually recessive, hence it only takes a single mutation to one of the alleles (to become dominant as it is a gain of function mutation) before a mutant phenotype is seen. Although, this is not true for all cancers, and sometimes the tumour
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