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Why RAS is such a dominant oncogene that makes it a good target for cancer therapy? How many different therapeutic approaches you can think of to target RAS in tumor cells? How to determine the in vivo efficacy of drug? ​

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Irving HeathcoteLv2
14 Feb 2018
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Related questions

Mutations in the genes that code for proteins in this pathway have been linked to various types of cance (i.e., RAS-pancreatic, BRAF-colorectal, MEK-melanoma, EGFR-lung). Of you were developing a new cancer drug, what would be an appropriate target protein for the new drug therapy? Justify your answer.

You have isolated a human tumor tht grows very rapidly. Design an experiment to show that there us a mutation in the RAS gene. The RAS gene promotes cell growth and dividsion when it is activated by activating the MAP kinase cascade. What type of mutation (s) to RAS might lead to transcription (unregulated growth) of cells? Hint: Where and how is RAS activated, and how is ot deactivated in normal cells? Prove tht your hypothesis is correct.

Mutations in the gene encoding Ras are often found in cancer. One of the mutations cancer cells often have is a change of the 12th amino acid from Glycine (normal Ras) to Asparagine (mutant Ras). Ras normally functions as an enzyme that can hydrolyze GTP. In other words, it catalyzes the reaction GTP <--> GDP + Pi. The mutation impairs the ability of Ras to hydrolyze GTP.

a. What are the properties of the Glycine found in the normal Ras? (Acidic, Basic, Nonpolar uncharged, or Polar Uncharged?) (See structure below).

b. What are the properties of the Asparagine found in the mutant Ras? (Acidic, Basic, Nonpolar uncharged, or Polar Uncharged?) (See structure below).

c. Compare the effect of wild-type and mutant Ras on the Ea (activation energy) and ∆G˚ (free energy change) of the reaction Ras catalyzes.

d. How is the activity of normal Ras regulated by environmental signals (which signal transduction pathway does it act in, and where does it act in that pathway)?

e. What would happen to the signal transduction pathway if Ras were unable to hydrolyze GTP? (Always on, always off, no effect)

f. How does Ras activity influence the cell cycle? [Hint, answer in terms of specific checkpoints].

g. Explain the effect of the mutation on cell proliferation in terms of your answers above.

h. Is the mutation sufficient to cause cancer? Explain your answer in terms of the two key properties of cancer cells.

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