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    Chemical-genetic study design elucidate Downstream Signal Chain

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    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.

    © BrainMass Inc. brainmass.com October 10, 2019, 8:15 am ad1c9bdddf
    https://brainmass.com/biology/absorption-distribution-metabolism-and-elimination/chemical-genetic-study-design-elucidate-downstream-signal-chain-616374

    Solution Preview

    Let's firstly break down the issues and identify the goal of the study:

    BCR-ABL+ bone marrow cells contribute to leukemia in CML patients.
    BCR-ABL activates KIT, KIT is also a positive regulator of bone marrow expansion
    Imatinib inhibits BCR-ABL
    Imatinib also inibits KIT
    Imatinib decreases measures of leukemia aggression in CML patients

    With this info, we can effectively rephrase the research question into something more specific:
    Does imatinib do so via BCR-ABL inhibition independent of KIT, or is KIT vital to the efficacy of imatinib in decreasing CML aggressiveness depend also on KIT functionality?

    To do this, what a researcher might have to do is design a CML model wherein KIT can be ...

    Solution Summary

    An example of how a chemical-genetic study design could help elucidate whether protein KIT is vital to BCR-ABL induced bone marrow expansion in leukemia.

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