Resistance To BCR-ABL Targeting Drugs
In the case of Gleevec (Imatinib), which targets the BCR-ABL fusion gene in chronic myeloid leukemia, resistance often develops through a mutation that changes the shape of the binding site of the drug. Sequential application of drugs can lead to the sequential evolution of resistance mutations to each drug in turn.
Gleevec is not as selective as was originally thought. It turns out that it targets other tyrosine kinase genes and can be used to control gastrointestinal stromal tumors (GISTs) that are driven by mutations in c-KIT. However, patients with GIST sometimes relapse with additional mutations in c-KIT that make the cancer cells resistant to Gleevec.
Read more about this topic: Somatic Evolution In Cancer, Somatic Evolution in Therapeutic Resistance
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