Abstract
A large majority of ALK rearranged lung cancer patients show significant clinical response to various generations of ALK tyrosine kinase inhibitors (TKI). Despite long lasting remissions resistance eventually develops to these therapies. Most resistance mechanisms are targeted including mutations in ALK kinase domain and ALK gene amplifications and others are off target involving other gene pathways. These mechanisms may cause conformational changes that alter drug binding or develop other escape mechanisms.
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