Imatinib is successful in treating BCR-ABL-positive chronic myelogenous leukemia (CML) patients. This is achieved by suppressing the expansion of BCR-ABL-positive bone marrow cells present in the patients. Besides BCR-ABL, imatinib also inhibits KIT, a receptor tyrosine kinase that can be activated by BCR-ABL and a positive regulator of expansion of bone marrow cells. These results complicate the interpretation that inhibition of BCR-ABL by imatinib is responsible for the observed efficacy in patients.
Please describe an experiment, with appropriate controls, that uses a chemical-genetic approach to address the question of whether inhibition of JUST BCR-ABL by imatinib is sufficient for the observed suppression of BCR-ABL-positive bone marrow cells.
This question was answered on: Sep 16, 2020
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