A single amino acid change in RAS eliminates its ability to hydrolyze GTP, even in the presence of a GTPase-activating protein (GAP). Roughly 30% of human cancers have this change in RAS. You have identified a small molecule that prevents the dimerization of a receptor tyrosine kinase that signals via RAS. Would you expect this molecule to be effective in the treatment of cancers that express this common, mutant form of RAS? Why or why not?

1. According to the question, when a change in an oncogenic gene is induced by a molecule, many types of cancer are expected to improve by inducing these new processes, so the answer is yes.

2. the process can be explained by the reaction binding to RTK that leads to the generation of RTK dimers, later it undergoes autophosphorylation and activation which triggers an activating response on RAS that is involved in the generation of cancer cells, when all these events occur, if the molecule interferes, it is expected that the response will not be triggered until the final result that would be the prevention of cancer