A research study indicated that an agent in cigarette smoke caused the silencing of the p53 gene, which is a tumour-suppressor. However, using sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.
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- 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…Loss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.Proto-oncogenes can be converted to oncogenes in a numberof different ways. In some cases, the proto-oncogene itselfbecomes amplified up to hundreds of times in a cancer cell.An example is the cyclin D1 gene, which is amplified in somecancers. In other cases, the proto-oncogene may be mutatedin a limited number of specific ways, leading to alterations inthe gene product’s structure. The ras gene is an example of aproto-oncogene that becomes oncogenic after suffering pointmutations in specific regions of the gene. Explain why thesetwo proto-oncogenes (cyclin D1 and ras) undergo such differentalterations to convert them into oncogenes
- The p53 protein was discovered through its association with SV40 T antigen and assumed initially to be an oncoprotein. a. What is the current consensus as the function of p53 and what evidence caused this change in view? b. How does the effect of mutation in the p53 gene differ from the effect of mutation in the RB gene what is the molecular basis for this difference ?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…A p53 knockout mouse in which both copies of p53 are defectivehas been produced by researchers. This type of mouse appears normalat birth. However, it is highly sensitive to UV light. Based onyour knowledge of p53, explain the normal appearance at birth andthe high sensitivity to UV light.
- In addition, when ARF is artificially expressed in normal cells, a rapid increase in p53 levels is observed. Studies have demonstrated that ARF, when expressed, is associated with Mdm2. When associated, the two proteins display a particular pattern of localization restricted to the nucleolus. Suggest a mechanism by which ARF leads to p53 build-up.Li- Fraumeni Syndrome (LFS) is a rare hereditary cancer disease due to a mutation in the TP53 gene. Propose a treatment strategy for LFS.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…
- 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.A research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.(46) A mutated form of protein p5x is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bin d to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteins