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A breakthrough in molecular biology — discovery of the fused BCR-ABL gene that drives cell proliferation in chronic myelogenous leukemia (CML) — led directly to development of a powerful new therapeutic agent, imatinib (Gleevec). Imatinib and two similar drugs, nilotinib (Tasigna) and dasatinib (Sprycel), inhibit the activity of the BCR-ABL fusion protein by binding to a particular site. However, malignant cells can develop mutations that engender resistance to these drugs.
An international team identified another binding site on BCR-ABL that can be targeted by a different class of drugs, which also inhibits the activity of BCR-ABL. When a member of this new class, GNF-5, was used in combination with imatinib or nilotinib, drug resistance mo…