Given what you have learned about tumor suppressors and proto-oncogenes, predict whether the following genes are likely to be tumor suppressors or proto-oncogenes. S-Cdk is likely to be a [Select] The inhibitor of Ras is likely to be a [Select]
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1. Hyperproliferation or cell cycle arrest; cell cycle arrest or accumulation of dna; hyperproliferation or growth stress increase or decrease
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- 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!Tumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367EThe 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.
- Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)Cancer Cells need A.I.R in order to survive and proliferate. What does this stand for? a. Activation of TSG's; Inactivation of oncogene; Replenishing of Telomeres b. Absorption of oncogenes; Inactivation of TRK's; Replenishing of Telomeres c. Activation of oncogenes; Inactivation of TGF's; Replenishing of Telomeres d. Activation of oncogene; Inactivation of TSG's; Replenishing of TelomeresIn a patient with a constitutively active receptor tyrosine kinase that increases the activity of PI3K, the administration of a drug that increases PTEN expression will likely inhibit tumorigenesis because; Group of answer choices PTEN prevents growth factor binding to RTK PTEN competitively inhibits the catalytic subunit of PI3K PTEN dephosphorylates PIP3 PTEN inhibits the dimerization of the regulatory subunit of RTKs
- What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.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)?A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesis
- A patient comes into your clinic exhibiting generic cancer symptoms. In order to help form a diagnosis, you ask about patient history and they tell you that they worked for years in an agricultural job, primarily in handling food for large bovine animals and then later working with insect pesticide treatment of grain fields. You decide to test for elevated levels of the environmental agent(s) in their body and focus your cancer diagnosis on based on the established associations of epigentic effects and cancer. O nickel and cadmium; stomach and skin cancer O benzene; breast, prostate and thyroid cancer O polycyclic aromatic hydrocarbons and benzene; lung, breast, stomach and skin cancer O arsenic and endocrine disruptors; skin, bladder, liver and kidney cancerChemotherapeutic agents can promote apoptosis in cancer cells by these mechanisms except; Group of answer choices Downregulating MCL1 expression Increasing BCL-2 expression Increased p53 expression Increased BIM (BH-3) expressionIn your own words: Describe the molecular mechanisms involved in P53’s role as a tumor repressor protein.