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Philipps-Universität Marburg
Abstract
In my research, I found that the compensatory activation of PI3K/AKT/mTor signaling pathway contributes early imatinib resistance in LAMA cell models. We also found that the auto/paracrine of GM-CSF by imatinib resistant leukemic cells confers to potent imatinib and nilotinib resistance. These findings may serve as a novel strategy to overcome disease resistance to imatinib.
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This item has been published with the following license: In Copyright