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- What is inflammation? Describe the main characteristics of inflammation. What characterizes chronic inflammatory disorders? What is the role of NFkB in inflammation and cancer? What are the mechanisms and strategies to inhibit excessive and chronic inflammation? answer should be one page longDescribe the mutational event that produces the MYC oncogene in Burkitt’s lymphoma. Why does the particular mechanism for generating oncogenic MYC result in a lymphoma rather than another type of cancer? Describe another mechanism for generating oncogenic MYC.5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…
- What are Ras protein and p53? How can mutations in the genes for these proteins contribute to cancer?1) A) List 15 drugs (monoclonal antibodies can be used) used clinically to treat cancer in humans. These targets must be signal transduction pathway components. B) For each drug, list the specific protein targeted. C) For each drug, describe the efficacy of treatment (i.e. what is the success rate in life extension) as well as appropriate cost of treatment whether it be per round or an average annual cost.For many years, targeted therapies for cancer treatment continue to be developed, however more and more patients are developing resistance to targeted therapies. Discuss one mechanism of resistance to targeted therapies for cancer and provide an example of how might creatively combat it using clinical concepts.
- Tissues and differentiation a)Explain what is meant by termination and differentiation ).b) Explain the difference between an oncogenic and a tumour suppressor gene and describe how they are involved in the onset of cancerOur government has finite funds to devote to cancer research.Discuss which of the following areas of research you think shouldreceive the most funding.A. Identifying and characterizing oncogenes and tumorsuppressorgenesB. Identifying agents in our environment that cause cancerC. Identifying viruses that cause cancer D. Devising methods aimed at killing cancer cells in the bodyE. Informing the public of the risks involved in exposure tocarcinogensIn the long run, in which of these areas would you expect successfulresearch to be the most effective in decreasing human mortalitydue to cancer?I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.
- Although cancer is not a contagious disease in humans or other vertebrates, there have been rare cases in which cancers have spread from one organism to another. Describe three cases of these contagious cancers and what conditions might have led to their appearance. For an introduction to this topic, see http:// www.cancer.org/cancer/cancerbasics/is-cancer-contagious.1. Describe & explain the pathophysiology of cancer based on the diagram. Reference: https://www.onlinebiologynotes.com/cancer-etiology-pathophysiology-types-diagnosis-and- treatment/ Acquired (environmental) DNA damaging agents: • chemical • radiation viruses Activation of growth- promoting oncogenes NORMAL CELL DNA Damage Failure of DNA repair Mutations in the genome of somatic cells Alteration of genes that regulate apoptosis Malignant neoplasm / Successful DNA repair CANCER Inherited mutations: • Genes affecting DNA repair • Genes affecting cell growth Expression of altered gene products and loss of regulatory gene products Inactivation of cancer suppresor genes Clonal expansion Additional mutations (progression) T Heterogeneitywhy EGFR play a role in CRC and other cancer?