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
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- #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.In your own words, explain how cancer cells differ from normal cells in regard to the following: Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)The best strategy for treating a specific type of human tumor can depend on identifying the type of cell that became cancerous to give rise to the tumor. For some tumors that have colonized a distant location (metastasized), identifying the parental cell type can be difficult. Because the type of IF protein expressed is cell-type-specific, using monoclonal antibodies that react with only one type of IF protein can help in this identification. What IF proteins would you produce monoclonal antibodies against to identify (a) a sarcoma of muscle cell origin, (b) an epithelial cell carcinoma, and (c) an astrocytoma (glial cell tumor)?
- You have two patients with pancreatic cancer. Patient 1 has a KRAS oncogenic mutation; a myc oncogenic mutation and has normal levels of P53. Patient 2 has normal KRAS expression: a myc oncogenic mutation and a tumor suppressor mutation in P53. You have the following therapeutics available Flavopiradol (a CDK inhibitor); CBP-93872 (a G2/M checkpoint inhibitor); Rigosertib; Oncorine; Nutlin a. Which patient would CBP-93872 be the most effective? Explain your answer. b. Which therapeutic(s) would not be expected to be effective in patient 2? For each, explain your answerDiscuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.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!
- Ras is a proto-oncogene that is within the EGF pathway. The EGF receptor can activate the cell division pathway only when the EGF ligand binds to the receptor. A gain of function mutation occurs in only one copy of the Ras gene. What are all the possible consequences of this? Select all that apply. Group of answer choices The cell will undergo constant cell division The cell will still be normal as only one copy of Ras is mutated. Both copies must be mutated for the cell to undergo constant cell division There will be an increase of EGF ligands present in the cell The EGF receptor will always be active even with no EGF ligands bound and activate the pathway Ras will always be active and activate the proteins downstream that will turn on cell division Ras will be under the influence of the EGF receptor and will only activate if the EGF ligand is bound to the receptorImagine that there are mutations in the CDK genes such that their gene products are nonfunctional. What effect would this mutation have on an immature unspecialized blood cell precursor found in the bone marrow? The cell would not be able to reproduce itself. The cell would complete the cell cycle using cyclins in the absence of CDKS. The cell would be able to replicate its DNA but not translate DNA into RNA. The cell would be able to enter mitosis but not complete it. The cell would still phosphorylate the CDK-associated target proteins, and would do so more quickly.Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell division
- #1) Hyperplastic growth are not cancerous yet but show a higher than normal proliferation rate. True False #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 situ #9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #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 decreasep53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such a familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply Group of answer choices None of the other answers effectively describes the situation If they get malignant cancer, somatic mutations will not have been a factor Their cancer will most likely arise in their germ cells, not their somatic cells Most cells in their body contain multiple cancer-causing mutations Every cell of their body contains a gain-of-function allele of an oncogene Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor gene