Which targeted therapy is used to treat CML by inhibiting BCR-ABL tyrosine kinase?

Prepare for the Hematologic, Immunologic, and Neoplastic Disorders Test. Study with flashcards and multiple-choice questions, each with explanations and hints. Get ready for your exam!

Multiple Choice

Which targeted therapy is used to treat CML by inhibiting BCR-ABL tyrosine kinase?

Explanation:
In CML, the disease is driven by the BCR-ABL fusion tyrosine kinase, which stays on continually and pushes leukemic cells to proliferate. A drug that directly inhibits this kinase can shut down the abnormal signaling and reduce leukemic cell growth. Imatinib does exactly that: it binds to the ATP-binding site of BCR-ABL, blocking its kinase activity and downstream signaling, leading to decreased proliferation and increased death of the malignant cells. This targeted approach was a major advance in CML therapy because it specifically interrupts the driver mutation. Rituximab, on the other hand, targets CD20 on B cells and is used in various B-cell lymphomas and some autoimmune diseases, not for inhibiting BCR-ABL. Methotrexate and hydroxyurea are not specific BCR-ABL inhibitors and act through different, non–BCR-ABL–focused mechanisms.

In CML, the disease is driven by the BCR-ABL fusion tyrosine kinase, which stays on continually and pushes leukemic cells to proliferate. A drug that directly inhibits this kinase can shut down the abnormal signaling and reduce leukemic cell growth. Imatinib does exactly that: it binds to the ATP-binding site of BCR-ABL, blocking its kinase activity and downstream signaling, leading to decreased proliferation and increased death of the malignant cells. This targeted approach was a major advance in CML therapy because it specifically interrupts the driver mutation.

Rituximab, on the other hand, targets CD20 on B cells and is used in various B-cell lymphomas and some autoimmune diseases, not for inhibiting BCR-ABL. Methotrexate and hydroxyurea are not specific BCR-ABL inhibitors and act through different, non–BCR-ABL–focused mechanisms.

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