Which of the following drugswould directly target the ability ofcancer cells to evade cell growthsuppressors? (evading the growthsuppressor hallmark)Anti-inflammatory drugsVEGF signalinginhibitorsCyclin-dependent kinaseinhibitorsTelomerase inhibitors

What is VEGF? Many cells generate vascular endothelial growth factor (VEGF), formerly known as…

Answered: would directly target the ability of…

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter14: Biotechnology And Society

Section: Chapter Questions

Problem 3QP

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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 controls
Chemotherapeutic 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) expression
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
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…
State the action(s) of each of the following signal molecules:a. IGF-1b. PDGFc. epidermal growth factord. IRS-1e. tumor necrosis factor
Some cancer cells are insensitive to typical chemotherapy. Research into the mechanisms underlying this insensitivity uncovered an ability by these cells to pump the treatment drug out of the cell against its concentration gradient. Additional drugs have been developed that inhibit the pump, thus trapping the chemotherapeutic agent inside to promote cancer cell destruction. The Figure shows what happens when two types of cells are treated with a 3H-labeled anti-cancer drug, paclitaxel. Two additional drugs, imatinib and nilotinib, are evaluated for their ability to overcome the cancer cells ability to pump out the chemotherapeutic agent. An asterisk (*) indicates a statistically significant difference from the cells receiving paclitaxel alone. Do the additional drugs seem to the effective in over-coming the pump? Which set of graphs (A or B) best supports your answer? Explain your answer.
Antibodies have two identical antigen-binding sites. Remarkably, antibodies to the extracellular parts of growth-factor receptors often lead to the same cellular effects as does exposure to growth factors. Explain this observation
Which are the Some Chemotherapies Target Cells Without Functional Tumor-Suppressor Genes
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
Can you explain how chemotaxis proteins work and the process that takes place with them? Thank You
In order for certain cancers to propagate, they require a growth factor known as Vascular Endothelial Growth Factor (VEGF). What does VEGF signal the cell to do and how does this promote the propagation of cancer cells?
Which of the following exert their cell signaling ability proteteolysis of other proteins? multiple answers A. RAS B. Epidermal Growth factor C. Notch Receptor D. TGF-Beta Receptor E. Estrogen Receptor

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would directly target the ability of cancer cells to evade cell growth suppressors? (evading the growth suppressor hallmark) Anti-inflammatory drugs VEGF signaling inhibitors Cyclin-dependent kinase inhibitors