Please explain the relationship between proto-oncogenes and the cell cycle. Then describe three different types of alterations in the genome in relation to proto-oncogenes that alter the cell cycle and cause cancer.
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Please explain the relationship between proto-oncogenes and the cell cycle. Then describe three different types of alterations in the genome in relation to proto-oncogenes that alter the cell cycle and cause cancer.
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- 1. a)Proteins that stimulate/promote progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. b)Proteins that inhibit progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. c)What is the difference between a proto-oncogene and an oncogene? d)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.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!You are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4B
- Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?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 regions#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.
- 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…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.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.
- Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, Bcl-2, telomerase, jun, andName 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.A cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .