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Which of the following are charcteristics you would expect of a circulating tumor cell that has undergone Epithelial-Mesenchymal Transition (select all that apply)?
A. Increased N-cahedrin expression
B. Increased resistance to apoptosis
C. Loss of ability to secrete fibronectin
D. High cytokeratin expression
E. Elevated PDGF Receptor Expression
Step by step
Solved in 3 steps
- Cancer cells may be more susceptible than normal cells to mitotic catastrophe in response to chemotherapeutic drugs because of which of the following (select all that apply)? A. They express unique receptors for those drugs on their surface B. They may be resistant to apoptosis C. Cancer cells have more efficient DNA repair mechanism than normal cells. D. Only cancer cells are actively dividing E. They may lack key G2/M checkpoint controlsWhich of the following cell-types are most likely to secrete Matrix Metalloproteases (MMPs) that remodel ECM near tumor (select all that apply)? A. Carcinoma Cells B. Mast cells C. Normal Epithelial Cells D. Macrophages E. FibroblastsWhich of the following statements are correct about cell signaling and proliferation in normal cells? more than one answer A. Cells require growth factors from other cells to proliferate B. Growth Factors must enter cell to signal cell growth C. Growth Factor Receptors can be oncogenes D. Protein Growth Factors can be Oncogenes E. Staurosporine is a potent inhibitor of Ser/Thr kinases and would be expected to inhibit Epidermal Growth Factor Receptor signaling
- Malignant tumor cells are characterized by all of the following properties except: A. loss of density-dependent (contact) inhibition B. reliance on aerobic respiration C. reduced dependence on aerobic respiration D. loss of anchorage dependence E. gain of unlimited proliferative potentialIf somatic tumors cause local regions in their vicinity to have an increased pOH, how is this strategic for the survival of the tumor? Select one: a. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. b. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. c. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. d. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. e. None of these.Which of the following modifications of the Epithelial Growth Factor Receptor (EGFR) would be proliferative of epithelial cells? multiple answers A. Mutation of active site residue responsible for tyrosine phosphorylation. B. Deletion of extracellular ectodomain C. Mutation in ectodomain that prevents binding of EGF D. Cell expresses EGF E. Mutation in promoter that increases expression of EGF receptor F. Dimerization of receptor without growth factor G. Mutation in EGFR promoter that decreases expression of receptor
- Which of the following statements are correct about tumors and metastasis (select all that apply)? A. The majority of cancer deaths are due to primary tumor B. Loss of basement membrane by tumor mass is strong predictor of metastasis potential C. The tissue stroma contributes to whether a tumor cell will metastasize D. The majority of life threatening tumors occur in epithelial tissues E. The tendency of a primary tumor to metastasize is similar across different tissue typesWhich of the following factors contributes to angiogenesis as a result of a tumor growth? Select all that apply: a. Increasing tumor's access to oxygen and nutrients b. Increasing tumor's ability for growth, invasion, and metastasis c. Increasing expression of proto-oncogenes for cancer cells d. Increasing expression of tumor-suppressor genes for cancer cellsWhich of the following are mechanisms by which cancer drugs work (select all that apply)? A. Inhibit activity of oncogene B. Promote apoptosis C. Promote terminal differentiation of cells D. Inhibit drug transporters E. Promote DNA damage.
- 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)?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.Cancer cells have a complex interaction with the cells of the immune system that are present in the stroma. The immune cells have the potential to destroy the tumor if it is recognized as aberrant tissue. Which one of the following statements correctly describes an interaction between cancer cells and the immune cells of the stroma? A. Tumors stimulate formation of new blood vessels—angiogenesis—promoting tumor survival. B. The tumor establishes an immunosuppressive environment by blocking white-cell activation. C. Tumors invoke an inflammatory reaction that blocks entry of immune cells into the stroma. D. Immune cells block tumor growth by providing signals that inhibit cancer cell proliferation.