Under normal physiological conditions, proto-oncogenes and tumor suppressors help control cell growth and proliferation. When mutated, these proteins contribute to the development of cancer. Briefly detail the molecular basis of this phenomenon
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Under normal physiological conditions, proto-oncogenes and tumor suppressors
help control cell growth and proliferation. When mutated, these proteins
contribute to the development of cancer. Briefly detail the molecular basis of this
phenomenon
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- The palladin gene, which plays a role in pancreatic cancer (see theintroduction to this chapter), is said to be an oncogene. Which of itscharacteristics suggest that it is an oncogene rather than a tumorsuppressorgene?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.For each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)
- 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.Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsTwist transcription factors (TF) play key roles in embryonic development and are largelyundetectable in normal adult tissues; however, their expression is reactivated during tumorprogression and correlates with invasive and metastatic lesions. Transcription of the Twistgene is activated by Wnt signals and the Twist TF represses the gene for E-cadherin.Answer the following questions as briefly as possible, based on what was presented in class,not an internet search (complex answers that go beyond class material may lose points)a. Outline the steps from the Wnt signal to the E-cadherin gene (inclusive);e.g., A → B → C (with some clarifications such as “binds to”, “activates”, “represses”)b. What are the normal cellular and embryonic (morphological) consequences of Twist expression?c. How would inappropriate expression contribute to cancer?
- The retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.In tumor cells obtained from patients with Burkittlymphoma, a cancer of the immune system’s B cells,the myc gene often appears close to one of the breakpoints of a reciprocal translocation between chromosomes 8 and 14. In this translocated position, myc is expressed at a higher-than-normal level. Scientists hypothesize that Myc protein overexpression in B cellscontributes to lymphoma formation.a. Explain how transgenic mice produced using pronuclear injection could be used to test this hypothesis. (Assume that you previously cloned a generegulatory region that is active specifically in Bcells throughout the life of the mouse.)b. Suppose you wanted to overexpress Myc only inthe immune cells of mice, starting at one week ofage. To restrict Myc transcription spatially, youwill use same promoter described in part (a). Torestrict Myc transcription temporally, you will usea cre transgene whose expression is controlled byheat shock (hs-cre). Describe the mouse you wouldcreate to accomplish…Explain why mutations in tumor suppressor genes are recessive (both copies of the gene must be defective for the regulation of cell division to be defective), whereas mutations in oncogenes are dominant.
- 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?Some cancers are consistently associated with the deletion of a particularpart of a chromosome. Does the deleted region contain an oncogene or atumor-suppressor gene? Explain.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!