Question 4 Cancer is heterogenous mass of cells. a. Describe what is meant by "clonal evolution of cancer" [6 marks] b. Summarise the methodology of whole-exome Next Generation DNA sequencing [4 marks] c. Describe an example showing how whole-exome DNA sequencing has improved our understanding of cancer [10 marks] Question 5 Our immune system must be able to respond to novel infectious agents throughout our lifetimes. In response to this, infectious organisms have developed ways of avoiding our immune system. a. Define positive selection [4 marks] b. Using the genetics of our immune system as an example, provide an example of how genes encoding parts of our immune systems have evolved increased genetic diversity to meet the threat of infection. Explain the functional significance of this high genetic diversity [8 marks] c. Describe a region of the SARS-CoV-2 viral genome that shows elevated genetic variability and provide a reason for the higher genetic variability within this region [8 marks]
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Clonal evolution of cancer refers to the process by which a single cell with genetic mutations acquires additional mutations over time, leading to the development of a heterogeneous population of cancer cells within a tumor. This process is driven by selective Show more…
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Cancer cells have a number of key features in common, which were described in class as a list and have also been put forth in a model of the Hallmarks of Cancer. For Question 4 (parts 1-4), match each description with the cancer hallmark to which it most applies. There is only one answer for each description, so pick the best option from the hallmarks listed. Not all the hallmarks will be used. In cell culture, cells are no longer subject to contact inhibition and growth in a monolayer, and will grow above the monolayer in clusters. [ Choose ] Cells divide in the absence of mitogen signalling and grow in the absence of growth factor stimulation. [ Choose ] Loss of functional p53 leads to loss of response to cellular stress and DNA damage signals. Evading apoptosis Cells maintain telomere length by expressing
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Match each cancer term with its most accurate definition. A. generally a protein that plays a role as a "switch" in some cell process B. an agent or substance that causes changes in DNA sequence C. an gene that when not mutated prevents the cell from dividing or growing too much D. an gene that is mutated and promotes cell growth and division E. an gene that when not mutated assists the cell in dividing and growing F. an agent or substance that promotes the formation of cancer G. changes in the DNA such as mutations as well as breaks in the molecule H. process to detect and address breaks in the DNA proto-oncogene mutagen carcinogen tumor suppressor gene oncogene DNA damage DNA repair regulator
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Part F - How does this study advance cancer research? Specialized proteins called cell cycle regulators, such as p53 and p21, regulate the progression of the cell cycle from one phase to the next. This progression through the checkpoints is strictly regulated and usually works without error. When errors do occur, they can have catastrophic consequences, including cancer. How did this study lend new evidence to our understanding of how genes regulate the cell cycle, giving us a better chance of developing successful cancer treatments? Mutations in the p53 and p21 genes lead to checkpoint deficits, specifically the G2-M checkpoint, linked to multiple types of cancer. These checkpoint deficits can be exploited in the development of targeted treatments. All cells deficient in p53 and p21 proteins proceed to mitosis after radiation exposure, and the cells have DNA content that differs from what would be expected. This chromosomal abnormality can be exploited in the development of targeted treatments. Mutations in the p53 and p21 genes play a crucial role at the S checkpoint of the cell cycle, preventing cells with DNA damage from entering mitosis. Targeting therapies to these proteins could improve efficacy of treatment.
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