A 42-year-old woman comes to the physician for a follow-up examination after two separate Pap smears have shown dysplastic epithelial cells. Results of a molecular diagnostic test show DNA that encodes high-risk versions of the human papillomavirus E6 and E7 proteins. The viral E6 protein binds to the cellular p53 tumor suppressor gene, causing it to be degraded. Which of the following best describes the mechanism by which the E6 protein causes cervical cancer? (A) Arrests the cell cycle (B) Enhances tissue invasion and metastasis (C) Inhibits telomerase expression (D) Prevents apoptosis (E) Sustains angiogenesis
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- Retroviruses can cause cancer, along with some viruses with DNA genomes. For example, herpes papillomavirus causes cervical cancer. The HPV genome encodes a protein called E6 that interferes with p53 function, and another protein called E7 that inhibits the function of Rb protein. Explain how HPV causes cancer. Are the viral E6 and E7 protein functions more similar to oncogenes or tumor suppressors?Describe 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.Human tumour viruses account for an estimated 12% to 20% of cancers worldwide and often establish persistent infections in the host. Explain how viruses contribute to cancer development.
- Our understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation.Explain why many oncogenic viruses contain genes whose products interact with tumor-suppressor proteins.Human Papillomaviruses has of many strains. Some of them cause warts while others can cause cancer. The question is why some strains cause cancer and others cause relatively harmless warts. Please mention the status of the viral genome (or parts of it), such as integrated or free, and the action of the viral oncogenes in terms of promoting cell division (when it would normally be controlled). And what proteins do the products of the viral oncogenes target? And also what is their normal function?
- What are the molecular mechanism of cancer development. What mechanisms get mutated into oncovirus?Under normal physiological conditions, proto-oncogenes and tumor suppressorshelp control cell growth and proliferation. When mutated, these proteinscontribute to the development of cancer. Briefly detail the molecular basis of thisphenomenonThe 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!
- 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…Hereditary retinoblastoma generally affects children in both eyes, while spontaneous retinoblastoma usually occurs during adulthood only in one eye. Explain the genetic basis for the epidemiological distinction between these two forms of retinoblastoma. Explain the apparent paradox: loss-of-function mutations in tumor-suppressor genes act recessively, yet hereditary retinoblastoma is inherited as an autosomal dominant.Name the six fundamental properties of malignant tumours. Which of these properties are amenable to study in a cell culture model of cancer and why?