Cancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.
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- Cancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.
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- What is the difference between a proto-oncogene and a tumor-suppressor gene?Benign tumors: a. are noncancerous growths that do not spread to other tissues b. do not contain mutations c. are malignant and clonal in origin d. metastasize to other tissues e. none of theseThe 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!
- 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.Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor geneWhich of the following is true of tumor suppressor genes? Group of answer choices a) If this gene is overactive, it becomes an oncogene b) If one of the alleles is mutated, there is usually little effect. Two inactivating mutations are usually required for loss of function (recessive mutation). c) If one copy is lost, the gene no longer functions (dominant mutation) d) Tumor suppressors genes usually cause mitosis or cell growth e) Tumor suppressor genes decrease apoptosis
- Metastasis occurs when cells from a primary tumor invade and colonize other tissues. Metastasis is a complex, multistep process. Tumor cells must lose adhesion with other tumor cells, invade local tissues and vessels, move through the circulation, leave the vessels, and finally, establish new colonies at distant sites. Tumor cells gain the ability to cross epithelial layers and migrate through tissues by mutations, although the nature of the mutations that drive metastasis is poorly understood. Mutations that block expression of the E-cadherin gene are thought to be an important step in metastasis. The absence of E-cadherin expression could affect metastasis by blocking cell adhesion directly, by releasing signaling proteins bound to the cytoplasmic domain of E-cadherin, or by both mechanisms. To better understand how loss of E-cadherin contributes to metastasis, scientists created two cell lines that differed in their expression of E-cadherin. One cell line was blocked for expression…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?D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…
- Compare and contrast oncogenes and tumor suppressors. Contrast oncogenes and proto-oncogenes. Describe the types of mutations that convert proto-oncogenes into oncogenes. Summarize some functions of common oncogenes in cell survival and uncontrolled growth. Contrast tumor suppressors to oncogenes. Describe the types of mutations in tumor suppressors that are found in common cancers. Summarize the functions of common tumor suppressors in cell survival and cell growth.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.D) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…