More About Gleevec
Ideally cancer treatments target specific weaknesses in the cell processes that lead to cancer. The drug Gleevec has been designed to disrupt the growth of leukemia cells by blocking a binding site of a key protein found only in tumor cells and not in normal cells.
The growth of leukemia cells is stimulated when the mutant cancer enzyme BCR-ABL phosphorylates a substrate protein. This occurs when BCR-ABL takes a phosphate group from a bound ATP molecule and transfers it to the substrate. This causes the substrate to change shape. It can then go on to stimulate leukenia cell growth.
Gleevec's shape mimics ATP, and binds to the same site on BCR-ABL that ATP normally occupies. Gleevec thus prevents phosphorylation of the substrate protein, and inhibits leukemia cell growth.
Knowing the genetic path that a particular cancer follows could someday help physicians better treat individual patients. By determining the genetic defects responsible for a specific cancer, physicians might be able to select the therapy that will be most effective at eliminating that cancer. Furthermore, each cancer-causing gene that researchers identify can serve as a target for the development of more specific therapies that will wipe out cancer cells while leaving healthy cells unharmed.
From lecture two of the 2003 From the 2003 Holiday Lectures Series "Learning From Patients: The Science of Medicine."
Gleevec Teaching Tips
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The 2003 Holiday Lectures Series "Learning From Patients: The Science of Medicine."
Director: Dennis Liu, Ph.D.
Scientific Direction: Bert Vogelstein, M.D.
Scientific Content: Satoshi Amagai, Ph.D.
Animator: Eric Keller