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Potential mechanisms of disease persistece on TKI. Which is the cause of Minimum residual disease ?

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#1 valiantchong


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Posted 07 February 2011 - 08:56 AM

Potential mechanisms of disease persistence on imatinib therapy.

(a) Enhanced drug efflux by ABCG2 (ATPase-binding cassette G2) and/or other transporters (green).

(B) BCR-ABL target amplification by increased BCR-ABL transcript levels or gene amplification; insufficient concentration of inhibitor to completely shutdown kinase activity.

© BCR-ABL kinase domain mutations renderpersistent cells insensitive to imatinib.

(d) Protection within bone marrow microenvironment; stromal cells surround persistent cells.

(e) Quiescent, noncycling cells in deep G0 are impervious to the pro-apoptotic effects of imatinib.

(f) BCR-ABL is efficiently targeted, but BCR-ABL kinase activity is
dispensable for persistent cell survival.

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