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Editorial
January 16, 2020

Optimizing Targeted Therapy for Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia

Author Affiliations
  • 1Texas Children’s Cancer Center, Baylor College of Medicine, Houston, Texas
JAMA Oncol. 2020;6(3):333-334. doi:10.1001/jamaoncol.2019.5849

In 1996, Druker and colleagues1 published the initial report on the inhibitory effects of a compound later named imatinib, a BCR-ABL inhibitor that reduced proliferation of BCR-ABL–positive chronic myeloid leukemia (CML) cells in vitro. The concluding paragraph of their report captures the compelling promise of targeted anticancer therapy: “This compound serves as an example of a drug that was rationally designed to inhibit the function of a specific protein when the protein’s function was known to be involved in the pathogenesis of a specific disease state. It is hoped that by directing therapy toward the underlying disease mechanism, this will result in more effective and less toxic therapies.”1(p565)

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