Dr. Clement shared the bad news with his patient. “I’m sorry,Oliver, but it appears that the Gleevec you have been taking is nolonger working against your cancer, and your white blood cells aregrowing out of control again. We’ll do some genetic testing toconfirm, but the most likely cause of this relapse is that theBCR-ABL gene has mutated once again, and that mutation has renderedthe protein resistant to the Gleevec you have been taking.” Dr.Clement sat in his office reviewing the most recent genetic testingresults with Oliver. “As I expected,” he said, “you have acquired aresistance mutation in BCR-ABL that is preventing Gleevec fromdoing its job. But the good news is, we have another drug,dasatinib, that should be able to counteract this mutation. I amgoing to call in a prescription for dasatinib that you should startright away.”

Oliver was skeptical. If Gleevec wasn’t working against hiscancer, what was so magical about this new drug, dasatinib?

What class of inhibitor is dasatinib?

Compare and contrast the function of dasatinib and the functionof imatinib/Gleevec.

Dasatinib, at nanomolar concentrations, inhibits the followingkinases: BCR-ABL, SRC family (SRC, LCK, YES, FYN), c-KIT, EPHA2,and PDGFRβ. Imatinib, at nanomolar concentrations, inhibitsprimarily BCR-ABL. How may these properties may affect Oliver’s newtreatment?