All four genes that are used to reprogram differentiated cells to function as pluripotent stem cells are transcription factors that are also known to be protooncogenes. Many of the early adult stem cell transplant experiments showed the development of cancers in the transplanted tissues. Explain.
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All four genes that are used to reprogram differentiated cells to function as pluripotent stem cells are transcription factors that are also known to be protooncogenes. Many of the early adult stem cell transplant experiments showed the development of cancers in the transplanted tissues. Explain.
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- 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 regionsThe C-myc gene is a proto-oncogene which is highly expressed in breast tissue and appears to cause proliferation of breast tissue and its elevated expression is associated with breast cancer. Based just on the ChIP data from the previous questions (also shown below), which of the three drugs (estrogen, tamoxifen and raloxifene) would you recommend for treating breast cancer? Justify your response and explain the potential side effects of each drug.Following are the characteristics of organoids, except: Organoids are in vitro 3D clusters of cells deriving exclusively from primary tissue or stem cells Organoids are capable of self-renewal and self-organization. 2D monolayer cultures are much closer to the in vivo situation than the organoids Spatially restricted cell-fate decisions contribute to self-organization in organoids.
- Proto-oncogenes can be converted to oncogenes in a number of different ways. In some cases, the proto-oncogene itself becomes amplified up to hundreds of times in a cancer cell. An example is the cyclin D1 gene, which is amplified in some cancers. In other cases, the proto-oncogene may be mutated in a limited number of specific ways, leading to alterations in the gene product’s structure. The ras gene is an example of a proto-oncogene that becomes oncogenic after suffering point mutations in specific regions of the gene. Explain why these two proto-oncogenes (cyclin D1 and ras) undergo such different alterations in order to convert them into oncogenes.Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.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?
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?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…
- Genetic tests that detect mutations in the BRCA1 and BRCA2 oncogenes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?Researchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?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!