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)
Identify all potential conflicts of interest that might be relevant to your comment.
Conflicts of interest comprise financial interests, activities, and relationships within the past 3 years including but not limited to employment, affiliation, grants or funding, consultancies, honoraria or payment, speaker's bureaus, stock ownership or options, expert testimony, royalties, donation of medical equipment, or patents planned, pending, or issued.
Err on the side of full disclosure.
If you have no conflicts of interest, check "No potential conflicts of interest" in the box below. The information will be posted with your response.
Not all submitted comments are published. Please see our commenting policy for details.
Rabin KR. Optimizing Targeted Therapy for Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia. JAMA Oncol. 2020;6(3):333–334. doi:10.1001/jamaoncol.2019.5849
Coronavirus Resource Center
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: