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19: What are 3
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- Isothiocyanates arè compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins DNA Damage p53 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells O Have no effect on progression of cervical cancer cells5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…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 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 p15INK4B1) Are NGN2-induced neurons (NGN2-iNs) the same as the cells in neural organoids? If not, how are they different? 2) Forced expression of the transcription factor neurogenin 2 (NGN2) induces human neurons, but to mature into electrophysiologically active neurons the require the presence of another cell type: what is that? 3)What kind of expression of NGN2 is associated with a central nervous system (CNS)-like cell? How do you know this?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 receptor
- Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth. a) What purpose does this forward…#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.Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.
- 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!1. True or Flase: Cells must only divide when they receive a signal to divide. 2. BRCA1 is a gene that codes for a tumor suppressor protein. If a person inherits a mutation in BRCA1, it greatly increases his or her risk of developing breast cancer. Are the cancer-causing mutations in the BRCA1 gene more likely to: a) increase expression of the gene b)decrease expression of the gene c)not affect the expression of the geneYou 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 answer
