Mutant tyrosine kinase signaling proteins are implicated in many types of human cancer. Hundreds of millions of dollars are required for the basic research and development of a new drug. Tyrosine kinase inhibitor drugs have been approved for cancer treatments by the U.S. Food and Drug Administration. What do you think would be some of the difficulties of finding these drugs given that similar kinases are active in normal cells? Do you think new medications of this type should be developed through government-sponsored research? Why or why not? If not, what alternatives do you propose?

Mutant tyrosine kinase signaling proteins are implicated in many types of human cancer. Hundreds of millions of dollars are required for the basic research and development of a new drug. Tyrosine kinase inhibitor drugs have been approved for cancer treatments by the U.S. Food and Drug Administration. What do you think would be some of the difficulties of finding these drugs given that similar kinases are active in normal cells? Do you think new medications of this type should be developed through government-sponsored research? Why or why not? If not, what alternatives do you propose?

Biology (MindTap Course List)

11th Edition

ISBN:9781337392938

Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Publisher:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Chapter6: Cell Communication

Section: Chapter Questions

Problem 16TYU

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You are a scientist studying two related congenital diseases, Noonan syndrome and Tiger syndrome. People with these syndromes are characterized by differences in heart development and skeletal morphology. Individuals with either syndrome are also susceptible to certain types of cancer, such as leukemia. Some cases of Noonan syndrome are caused by dominant activating variants of the MAP kinase-kinase-kinase protein Raf. The genetic basis of Tiger syndrome is unknown. Your team is involved in a clinical trial, which finds that drugs that inhibit Raf are associated with improved outcomes in cancer patients with Noonan syndrome. You find that Tiger syndrome patients also respond to the treatment, so you sequence the Raf gene in several patients, but find no mutations. Based on what you know about the MAP kinase pathway, you sequence the Sos gene in Tiger syndrome patients. You find that 5 out of 10 patients in your trial have a SNP that changes the amino acid Thr266 to Lys (T266K).…
Two protein kinases, barley kinase and hops kinase, function sequentially in an intracellular signaling pathway. If either kinase contains a mutation that permanently inactivates it, no response is seen in cells when an extracellular signal is received. A mutation that permanently activates barley results in a response even when there is no extracellular signal. You characterize a double mutant in which hops has the inactivating mutation and barley has the activating mutation. You observe that a response is seen in the double mutants even in the absence of an extracellular signal. In the normal signaling pathway, does barley phosphorylate hops or does hops phosphorylate barley? Briefly explain your answer.
If you have a protein kinase that is regulated by both small molecule inhibitors as well as by phosphorylation, and is part of a cooperative enzyme complex that works as part of a larger pathway involving kinase and GTPase proteins please explain where on this protein regulation could occur, how different types of inhibition could control the function of the protein as well as the function of the complex, and how the protein could regulate other proteins. (This question was previously answered but it was answered incompletely mentioning an herbicide developed in the 1950's. Apparently, it was a plagiarized excerpt from an NCBI article. This is a repost for a full and complete answer. Thank you so much for your help! :) )
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