Lung cell cancers are often associated with genetic changes in the EGFR/MAPK signaling pathway. One of the anti-cancer drugs that can be used to treat lung cancer inactivates the EGFR receptor at the plasma membrane. Which of the following cancers can be effectively treated with this drug? Cancers caused by Ras-GOF mutations Cancers caused by MAPKKK hyperactivation All of the options are correct Cancers caused by MAPK hyperactivation Cancers caused by EGFR over-expression

Lung cell cancers are often associated with genetic changes in the EGFR/MAPK signaling pathway. One of the anti-cancer drugs that can be used to treat lung cancer inactivates the EGFR receptor at the plasma membrane. Which of the following cancers can be effectively treated with this drug? Cancers caused by Ras-GOF mutations Cancers caused by MAPKKK hyperactivation All of the options are correct Cancers caused by MAPK hyperactivation Cancers caused by EGFR over-expression

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 2VCQ: Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means...

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Aberrant signaling through the Ras-BRaf-MAPK signal transduction pathway drives many cancers. This makes the pathway an attractive drug target, and many small molecules have been developed that target either Ras, BRaf or MAPK. In malignant melanoma, one mutation in particular, where valine 600 of Braf is mutated to a glutamic acid (V600E), is found in the majority of cases. This mutation makes BRaf activation independent of upstream Ras activity. Would a small molecule that targets Ras be effective in a melanoma case driven by Braf V600E? Explain your answer.
Which of the following mutations would produce a form of the Ras protein that would be more difficult to inactivate than normal Ras? Briefly explain your reasoning.(i) A mutation that allows Ras to cleave (hydrolyze) GTP more rapidly than usual(ii) A mutation that causes Ras to bind Ras-GAP more tightly than usual(iii) A mutation that causes Ras to cleave (hydrolyze) GTP more slowly than usual
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
what protein is phosphorylated by Raf in the Ras/MAP kinase signal transduction cascade? I put ERK2 and ERK1 but was partially incorrect, what was the part I messed up on that would be correct? I know that one of the two is there but correct me if i'm wrong
Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.
Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?
do you have any clues? GAP protein helps hydrolyze the GTP to GDP in RAS protein. Argenine 789 residue in GAP protein interacts with GTP in RAS protein. However, Arg 789 is mutated to Alanine. which are true or false? ____We expect Ala789 GAP to have no consequence for cell growth or survival signaling. ____Arg789 stabilizes the T-loop of GAP in the outward (active) position, so we expect Ala789 GAP to have no kinase activity. ___Arg789 participates in the GTP hydrolysis reaction carried out by RAS, so we expect RAS to be catalytically inactive when partnered with Ala789 GAP. ____Arg789 binds in the major groove of the DNA double helix, so we expect Ala789 GAP to be inactive as a transcriptional regulator. __Arg789 interacts with RAS switch 1 and switch 2 regions, so we expect the RAS switch to fail with Ala789 GAP. ____The RAS switch would be locked in the OFF position by Ala789 GAP, so we expect no constitutive RAS signaling and hence no risk of this tumor metastasizing. ____The…
Which of the following are characteristics of “small” monomeric Ras GTPases? A. Membrane bound B. Act as molecular switches between GTP & GDP C. They interact with receptors directly to regulate upstream events D. They are activated upon GTP binding E. None of the above
We saw that most cancer mutations in the ras/mapk pathway occur upstream of mapk rather than in mapk itself. what might be a reason for that?
The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.
We have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPase
A certain group of Brec-MUT cells expresses low levels of protein A, unlike the high expression levels of most Brec-MUT cells. Researchers determine that the cells have an excess of ATP and that there are no mutations in the gene encoding protein A. Describe a change in the Brec signaling pathway that would lead to the decreased expression of protein A even in the presence of Brec-MUT. Explain why B is able to bind to Brec but not to A.