Point mutations in multiple tumor suppressor proteins have been linked to cancer. For example changes in the gene for adenomatous-polyposis-coli protein (APC gene) may result in colorectal cancer. Consider the following DNA sense strand. 3'-TAC CGG TTG TGA AGC TGA ATC-5'
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- 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.Our understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? What is an oncogene? How does if differ from a proto-oncogene? Why are retroviruses prone to accumulating oncogenes? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formationA 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
- 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 how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?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…
- Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such as familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply a) If they get malignant cancer, somatic mutations will not have been a factor b) Their cancer will most likely arise in their germ cells, not their somatic cells c) None of the answers effectively describes the situation d) Every cell of their body contains a gain-of-function allele of an oncogene e) Most cells in their body contain multiple cancer-causing mutations f) Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor geneName two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.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.
- 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…For the following diseases, describe the best technique for diagnosing them. Please make sure you include how you would tell someone with the disease from someone without the disease. B. Factor V Leiden thrombophilia is caused by a point mutation at position 1691 in exon 10 of the Factor V clotting factor gene that changes an arginine into a glutamine. This change removes one of the cleavage sites for activated protein C and leads to an increased tendency to clot.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.