Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)
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A: Answer
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- Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.
- Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.The p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.
- Describe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.Given the following scenario, indicate if this will ‘promote’ or ‘prevent’ cancer development: An over-expression of Bcl-2
- Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?The Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!Of the following choices a loss of function mutation would most lukely contribute to cancer onset if the mutant gene codes for a : telomerase tumor suppressor protein ATP synthesis enzyme RNS binding protein