Gefitinib has been shown to be an effective tyrosine kinase inhibitor in a fraction (~$10$%) of non-small cell lung cancer patients.
These patients are characterized as having a mutation (usually a deletion or missense) in the EGFR gene affecting the ATP-binding site.
I have two questions:
-- How does gefitinib impede the proliferation and apoptosis pathway? Does it in effect "ace out" the binding of EGF? If this is correct, how does it accomplish that? If not, I would appreciate a brief explanation as to what the successful mechanism is.
-- It seems that (similar to imatinib, another tyrosine kinase used to treat CML) successfully treated patients tend to relapse after a period of time. Why is this?